Startseite Understanding risk factors and prognosis in diabetic foot ulcers
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Understanding risk factors and prognosis in diabetic foot ulcers

  • Jixue Wang , Xirui Yang , Tao Zhou , Haitao Ma , Xingxing Yuan und Shuxun Yan EMAIL logo
Veröffentlicht/Copyright: 8. August 2025
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Open Life Sciences
Aus der Zeitschrift Open Life Sciences Band 20 Heft 1

Abstract

Diabetic foot ulcer (DFU) is a severe and prevalent complication of diabetes mellitus, posing substantial risks to patient health and increasing healthcare burdens globally. These chronic wounds often result from a complex interplay of factors, including neuropathy, ischemia, infection, immune dysregulation, and vascular dysfunction, leading to significant morbidity and, in severe cases, amputation. Effective management of DFUs necessitates a comprehensive understanding of their risk factors and prognostic indicators. This review provides an in-depth examination of the various risk factors and prognostic markers associated with DFUs, integrating insights from cellular mechanisms, emerging biomarkers, omics-based research, serological studies, and clinical assessments. We explore the underlying biological processes, such as the impact of chronic hyperglycemia, oxidative stress, inflammation, impaired angiogenesis, and the role of the microbiome in DFU development. The role of serological markers, including inflammatory and glycemic indicators, in predicting DFU risk and progression is discussed. Additionally, clinical markers and advanced assessment tools, such as ulcer grading systems and imaging technologies, used to evaluate DFU severity and healing are reviewed. By synthesizing these diverse perspectives, this review aims to offer a holistic view of DFU management, highlighting how understanding the interplay of risk factors and prognostic markers can lead to improved prevention strategies and personalized therapeutic interventions.

Keywords: diabetic foot ulcers; risk factors; prognostic markers; wound healing

1 Introduction

Diabetic foot ulcers (DFUs) are a severe and prevalent complication of diabetes mellitus, affecting approximately 15–25% of individuals with diabetes at some point in their lives [1]. These chronic wounds are often the result of a complex interplay of factors, including peripheral neuropathy, impaired blood flow, immune dysregulation, repeated trauma, and microbial imbalance, leading to significant patient morbidity and increased healthcare costs. DFUs are associated with a high risk of infection, which can lead to limb amputation if not managed appropriately [2].

The clinical importance of DFUs extends beyond the immediate health consequences, as they contribute to prolonged hospital stays, frequent surgical interventions, and substantial healthcare expenditures [3,4]. Additionally, DFUs can severely impact patients’ quality of life by limiting mobility and increasing the risk of psychological distress. Psychological comorbidities such as depression and anxiety are commonly reported and may negatively influence treatment adherence and wound outcomes. Given these challenges, there is an urgent need for a better understanding of the factors that contribute to the development and progression of DFUs, as well as the indicators that can predict their outcomes [5].

Research into the risk factors and prognostic markers for DFUs is crucial for advancing prevention and treatment strategies. Key risk factors include inadequate glycemic control, which accelerates the formation of advanced glycation end-products (AGEs) and exacerbates oxidative stress; peripheral neuropathy, which impairs sensory perception and increases the risk of unnoticed injuries; and peripheral vascular disease, which compromises blood flow and impedes wound healing [6–8]. Additionally, inflammatory responses play a significant role in the pathogenesis of DFUs, with elevated levels of pro-inflammatory cytokines being associated with poor ulcer outcomes. In addition, impaired angiogenesis and endothelial dysfunction, chronic inflammation mediated by immune cells such as macrophages, and elevated oxidative stress biomarkers (8-hydroxy-2′-deoxyguanosine [8-OHdG], malondialdehyde [MDA]) have been increasingly recognized as central contributors to DFU pathogenesis.

Serological markers such as C-reactive protein (CRP) and glycated hemoglobin (HbA1c) provide valuable information about systemic inflammation and long-term glycemic control, respectively [9–11]. Emerging biomarkers, including microRNAs and cytokine panels, show potential for improving prognostic accuracy. Clinical assessment tools, including ulcer grading systems, pressure mapping, and advanced imaging modalities such as optical coherence tomography and hyperspectral imaging, help evaluate the severity of DFUs and guide treatment decisions. Furthermore, omics-based approaches – especially transcriptomics, proteomics, and single-cell analyses – are offering new insights into cellular heterogeneity and disease mechanisms.

This review aims to provide a comprehensive analysis of the risk factors and prognostic indicators associated with DFUs. By integrating insights into the underlying mechanisms, serological profiles, and clinical evaluation techniques, the review seeks to offer a detailed perspective on how these factors contribute to DFU development and progression. Ultimately, this approach will support the development of targeted interventions and personalized treatment strategies to improve patient outcomes and reduce the burden of DFUs.

2 Mechanisms of DFU

DFUs are a multifaceted complication of diabetes mellitus, arising from a combination of metabolic, vascular, immunological, and microbiological disruptions that collectively impair normal cellular and tissue functions. A thorough understanding of these mechanisms is crucial for effective prevention, diagnosis, and personalized treatment [12].

One of the primary contributors to DFU development is chronic hyperglycemia, which significantly impacts cellular function [12,13]. The persistent high blood glucose levels lead to the formation of AGEs. These AGEs result from the non-enzymatic reaction between glucose and proteins, lipids, or nucleic acids [14]. AGE accumulation impairs the extracellular matrix (ECM), activates the receptor for AGEs (RAGE) pathway and triggers inflammation and oxidative stress, all of which exacerbate tissue injury and delay healing [15].

Oxidative stress is another critical factor in the pathogenesis of DFUs. Chronic hyperglycemia increases the production of reactive oxygen species (ROS), which cause cellular damage through the oxidation of lipids, proteins, and DNA. This oxidative damage impairs cellular function and triggers inflammatory responses that further complicate wound healing [16]. Oxidative stress biomarkers such as 8-OHdG and MDA have been identified in DFU tissues and are being explored for clinical relevance.

Inflammation plays a significant role in DFU development and progression. Elevated levels of inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) are commonly observed in DFU wounds [17,18]. These cytokines perpetuate a chronic inflammatory state, which impairs tissue repair by promoting the breakdown of ECM components and hindering normal wound healing processes. Macrophage polarization imbalance (M1 over M2) and impaired neutrophil clearance are now recognized as hallmarks of delayed healing in DFU.

Several interrelated signaling pathways are dysregulated in DFUs, contributing to impaired healing through chronic inflammation, oxidative stress, and tissue remodeling defects. The nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway is a central mediator of sustained inflammation in DFU wounds. Hyperglycemia, AGE–RAGE interaction, and ROS can activate the NF-κB complex, which translocates to the nucleus and induces the expression of pro-inflammatory genes, including TNF-α, IL-6, and MMP-9. Persistent NF-κB activation prevents resolution of inflammation and disrupts normal wound healing [19].

The transforming growth factor-beta (TGF-β/Smad) signaling pathway plays a critical role in tissue repair by promoting fibroblast proliferation, ECM production, and re-epithelialization. In DFU, TGF-β signaling is often suppressed or dysregulated, leading to reduced collagen I and III synthesis and impaired granulation tissue formation. Moreover, crosstalk between TGF-β and inflammatory pathways further complicates wound resolution [20].

Vascular impairment is closely associated with defects in the VEGF/PI3K–Akt pathway, which normally promotes endothelial cell survival, proliferation, and angiogenesis. In diabetic conditions, VEGF signaling is attenuated or uncoordinated, impairing neovascularization and oxygen delivery to ischemic tissue [21].

Excessive matrix metalloproteinase-9 (MMP-9) expression, often induced by TNF-α and NF-κB signaling, degrades ECM components such as collagen and laminin, disrupting the structural scaffold required for cell migration and wound closure. The imbalance between MMP-9 and its inhibitor TIMP-1 (tissue inhibitor of metalloproteinases) exacerbates ECM degradation. The Nrf2 pathway, which orchestrates the cellular antioxidant response, is often suppressed in DFU. Nrf2 regulates genes encoding antioxidant enzymes such as HO-1 and NQO1. Its reduced activity in diabetic tissues leads to elevated oxidative stress, contributing to cellular injury and chronic inflammation.

Changes in the ECM also contribute to the pathophysiology of DFUs. Diabetes alters the ECM’s structural and functional properties by disrupting the balance between matrix degradation and synthesis [22]. The impaired ECM remodeling results in a dysfunctional matrix that is less effective in supporting wound healing. Changes in ECM components, such as collagen and glycosaminoglycans, contribute to the chronic nature of DFUs and delay healing.

Neuropathy, a common complication of diabetes, further complicates DFU development. Diabetes adversely affects the production and function of neurotrophic factors essential for nerve growth and repair [23]. Reduced levels of these factors impair nerve regeneration and contribute to peripheral neuropathy, which diminishes sensory feedback. Consequently, patients with diabetic neuropathy are less likely to detect and respond to injuries, increasing the risk of ulceration. Additionally, neuronal apoptosis, or programmed cell death, plays a role in diabetic neuropathy [24,25]. The increased loss of sensory nerves due to apoptosis reduces the ability to sense potential injuries or pressure on the feet. This decreased sensory perception leads to delayed detection of wounds and further promotes the development and persistence of DFUs.

Recent advances in multi-omics technologies, including transcriptomics, proteomics, metabolomics, and single-cell RNA sequencing (RNA-seq), are uncovering new regulatory networks and cell-specific responses. For example, microRNAs such as miR-21 and miR-146a have been shown to modulate inflammation and angiogenesis in DFU contexts. Epigenetic modifications, including DNA methylation and histone acetylation, are also being explored as potential therapeutic targets.

To facilitate clinical translation, it is essential to distinguish biomarkers that are clinically validated from those still in early-stage research. While markers like HbA1c, CRP, and MMP-9 have established roles in assessing DFU severity and prognosis, others, such as exosomal microRNAs or single-cell-derived gene signatures, require further validation.

In summary, the pathophysiology of DFUs involves a complex network of metabolic dysregulation, oxidative stress, chronic inflammation, vascular and neural impairment, immune dysfunction, and microbiome imbalance. Table 1 summarizes the interconnected mechanisms and their contributions to DFU progression.

Table 1

Different mechanisms and their impacts on DFUs

Possible mechanism Description Impact on DFUs Reference
Chronic hyperglycemia Formation of AGEs Damages ECM, impairs tissue repair, exacerbates inflammation [26]
Oxidative stress Increased production of ROS Cellular damage, triggers inflammation, worsens healing [27]
Chronic inflammation Elevated inflammatory mediators (TNF-α, IL-1β, IL-6) ECM breakdown, impairs tissue repair, hinders healing [15]
ECM changes Disruption in ECM degradation and synthesis Dysfunctional matrix, delays healing [28]
Neuropathy Reduced neurotrophic factors, impaired nerve regeneration Diminished sensory feedback, increased ulcer risk [14]
Neuronal apoptosis Increased programmed cell death in sensory nerves Reduced injury detection, promotes DFU development [6]

3 Serological markers

Serological markers are crucial for assessing disease severity, predicting prognosis, and guiding treatment decisions, helping to optimize patient management and improve clinical outcomes. Serological markers are valuable tools for assessing the risk, prognosis, and management of DFUs. These markers provide insights into the systemic conditions that influence ulcer development and healing [29].

Inflammatory markers are critical in assessing the inflammatory status associated with DFUs, and their role in disease progression is well established. CRP is a widely used inflammatory marker that increases in response to acute and chronic inflammation. In DFU patients, elevated CRP levels often correlate with the severity of inflammation and can indicate poor wound healing outcomes. Monitoring CRP levels helps clinicians gauge the inflammatory response and adjust treatment strategies accordingly [30]. Another important inflammatory marker is the erythrocyte sedimentation rate (ESR), which serves as an indicator of chronic inflammation [31]. Elevated ESR levels reflect ongoing inflammatory processes and provide valuable information regarding the inflammatory burden in DFU patients.

Glycemic markers are integral in understanding the relationship between blood glucose control and DFU risk. HbA1c is a key marker for long-term glycemic control, reflecting average blood glucose levels over the past 2–3 months. High HbA1c levels are associated with an increased risk of DFU development and poor healing outcomes [29,32]. Effective glycemic management plays a critical role in reducing the risk of DFUs and promoting wound healing, as poorly controlled blood glucose impairs immune function and tissue repair mechanisms. Additionally, acute fluctuations in blood glucose levels can significantly exacerbate tissue damage and delay healing, making blood glucose monitoring a critical component of DFU management.

Other serum markers provide further insights into the metabolic and nutritional status of DFU patients. Markers of insulin resistance, such as the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), are key in evaluating insulin resistance, a common condition in diabetic patients [33,34]. Elevated HOMA-IR levels are linked to an increased risk of DFUs and can help predict ulcer development. Furthermore, vitamin D deficiency has been implicated in both impaired immune function and poor wound healing in DFU patients. Assessing vitamin D levels can provide additional information on the nutritional status and overall health of DFU patients, aiding in the development of more effective treatment plans [35,36].

4 Omics markers

Omics technologies offer a comprehensive approach to understanding the molecular and cellular changes involved in DFUs. These technologies analyze large-scale datasets of genes, proteins, and metabolites, providing insights into the complex biological processes underlying DFU pathogenesis [37].

Genomic studies are essential in investigating the role of genetic variations and mutations in DFU risk. By employing genome-wide association studies, researchers have identified several genetic loci associated with diabetes and its complications, including DFUs. These genetic variations can influence susceptibility to DFUs by affecting critical processes such as inflammation, oxidative stress, and ECM remodeling. Identifying these genetic factors not only aids in pinpointing individuals at higher risk but also contributes to the development of more precise, personalized prevention strategies [38].

Transcriptomics, which examines gene expression profiles, provides critical insights into the molecular response to DFUs. Techniques like RNA-seq allow for the simultaneous analysis of thousands of genes. Changes in gene expression related to DFUs often reveal alterations in pathways involved in inflammation, wound healing, and cellular stress. For example, increased expression of inflammatory cytokines and decreased expression of wound-healing genes have been commonly observed in DFU tissues. These data can help identify potential therapeutic targets and biomarkers for managing DFUs [39].

Proteomics provides a detailed analysis of the entire set of proteins expressed in cells, tissues, or organisms, offering deeper insights into the molecular underpinnings of DFU pathogenesis. Mass spectrometry-based proteomics enables the identification and quantification of proteins involved in DFU progression. Proteomic analyses have highlighted several proteins linked to inflammation, oxidative stress, and ECM remodeling. For example, changes in levels of MMPs and TIMPs have been associated with impaired ECM remodeling and delayed wound healing. Proteomics helps uncover biomarkers reflecting disease processes and guides the development of targeted therapies [40].

Metabolomics involves analyzing the complete set of metabolites – small molecules involved in metabolic processes [28]. Profiling metabolites in DFU patients can reveal alterations in metabolic pathways related to glucose metabolism, oxidative stress, and inflammation. Techniques like mass spectrometry and nuclear magnetic resonance spectroscopy are used to identify and quantify these metabolites. Observations of changes in metabolites related to oxidative stress or glycation in DFU patients offer insights into disease mechanisms and help identify novel biomarkers for diagnosis and prognosis.

Lipidomics, the study of lipid profiles, also plays a crucial role in understanding DFUs. Changes in lipid composition and concentrations have been linked to inflammation and oxidative stress in DFUs [41,42]. By analyzing lipid profiles, researchers can uncover specific lipid species altered in DFUs, providing a deeper understanding of lipid-related mechanisms that contribute to disease development and progression.

Overall, omics technologies – encompassing genomics, transcriptomics, proteomics, metabolomics, and lipidomics – offer a powerful toolkit for exploring the molecular and cellular changes associated with DFUs. These approaches provide valuable insights into disease mechanisms, identify potential biomarkers, and hold significant potential for the development of personalized prevention and treatment strategies.

5 Clinical markers and assessment indicators

In the management of DFUs, clinical markers and assessment indicators play a crucial role in evaluating the condition and guiding treatment [43]. Foot examination and scoring systems are essential for assessing DFUs. Various ulcer grading systems, such as the Wagner classification and the University of Texas system, provide a structured approach to evaluate the severity of foot ulcers [44]. These systems help standardize the assessment and guide treatment decisions. Additionally, foot pressure assessments measure plantar pressure to identify areas at risk of developing ulcers, aiding in preventive care and reducing ulcer incidence.

The status of wound healing is another critical aspect of DFU management. Key indicators include the healing rate, which measures the progress of ulcer closure over time, and the time to healing, which is a crucial clinical parameter reflecting how quickly an ulcer is expected to heal. Monitoring these factors helps in evaluating treatment efficacy and predicting patient outcomes. Table 2 provides a comprehensive summary of serological, omics, and clinical markers used to assess, manage, and understand DFUs Figure 1.

Table 2

Overview of markers for DFUs: Serological, omics, and clinical

Category Marker type Specific markers Description Reference
Serological markers Inflammatory markers CRP Indicates inflammation; elevated levels correlate with DFU severity and poor healing outcomes [13]
ESR Reflects chronic inflammation and overall inflammatory burden [45]
Glycemic markers HbA1c Reflects long-term blood glucose control; high levels associated with increased DFU risk [46]
Blood glucose levels Acute fluctuations impact DFU risk and healing [44]
Insulin resistance HOMA-IR Evaluates insulin resistance; elevated levels linked to DFU risk [29]
Nutritional mar Vitamin D Deficiency associated with poor immune function and wound healing [31]
Omics markers Genomics Genetic variants: TCF7L2, PPARG, KCNJ11 Genes associated with diabetes and DFU susceptibility [12]
Inflammatory genes: IL6, TNF, IL1B Influence inflammation in DFUs [24]
Transcriptomics Inflammatory cytokines: IL6, TNF, IL1B Increased expression in DFU tissues [23]
Wound healing genes: VEGF, MMP-9, TIMP-1 Decreased expression in DFU tissues [15]
Proteomics Inflammatory proteins: TNF-α, IL-1β, IL-6 Associated with inflammation and wound healing [3]
ECM remodeling proteins: MMP-9, MMP-2, TIMP-1 Involved in ECM changes [39]
Metabolomics Glucose metabolites: Fructosamine, 3-DG Indicators of glucose metabolism and oxidative stress [22]
Oxidative stress metabolites: 8-OHdG, MDA Reflect oxidative damage [25]
Lipidomics Inflammatory lipids: Arachidonic acid, 5-HETE Linked to inflammation and oxidative stress [25]
Metabolic lipids: Ceramides, sphingolipids Associated with metabolic disturbances [47]
Clinical markers Foot examination Wagner classification System for grading ulcer severity [46]
University of Texas classification Grading system for ulcer severity and depth [17]
Foot pressure Plantar pressure measurements Identifies areas at risk for ulcer development [29]
Wound healing status Healing rate Measures ulcer closure progress [16]
Time to healing Reflects how quickly an ulcer is expected to heal [46]
Figure 1 Core pathogenic axis of DFUs.
Figure 1

Core pathogenic axis of DFUs.

The interactions between TGF-β, MMP-9, VEGF, IL-6, NF-κB, and CRP play crucial roles in the pathogenesis and healing process of DFUs. TGF-β promotes collagen synthesis during wound healing, while MMP-9 regulates ECM degradation. VEGF enhances angiogenesis to improve local blood flow, IL-6 modulates the inflammatory response, and NF-κB influences immune responses by regulating the expression of inflammatory mediators. CRP, as an acute-phase reactant, reflects systemic changes in the inflammatory state, and these molecules are closely involved in the pathology of DFUs.

6 Discussion

DFUs present a complex challenge in diabetes management, with their development and progression influenced by a range of interrelated factors. [45]. The mechanisms underlying DFUs reveal the profound impact of chronic hyperglycemia, which leads to the formation of AGEs. These AGEs accumulate and cause damage to the ECM, disrupting tissue repair and exacerbating inflammation. Concurrently, oxidative stress, characterized by increased production of ROS, further contributes to cellular damage and impairs the wound healing process [48,49]. This combination of AGEs and oxidative stress creates a detrimental environment for wound healing, highlighting the critical need for effective glycemic control and potential antioxidant therapies to manage DFUs [47].

For the mechanism of DFU, multiple interrelated factors contribute to its onset and delayed healing, including metabolic dysfunction, neuropathy, vascular impairment, chronic inflammation, and dysregulated molecular signaling. Persistent hyperglycemia leads to the formation of AGEs, oxidative stress, and impaired cellular repair, while diabetic neuropathy causes sensory loss, motor dysfunction, and autonomic disturbances, increasing the risk of unnoticed injuries and skin breakdown. Concurrently, both macrovascular and microvascular complications result in tissue ischemia and hinder the delivery of oxygen, nutrients, and immune cells. Chronic inflammation, marked by elevated IL-6, TNF-α, CRP, and sustained NF-κB activation, impairs normal wound resolution. Key molecular players such as TGF-β, MMP-9, VEGF, and CRP are involved in ECM remodeling, angiogenesis, and immune regulation but are often dysregulated in the diabetic environment. The wound microenvironment – characterized by hypoxia, high glucose levels, and bacterial biofilms – further disrupts the healing cascade, prolonging the inflammatory phase and impairing tissue regeneration. These complex mechanisms collectively underlie the pathogenesis and therapeutic challenges of DFUs [50].

Peripheral neuropathy complicates DFU management by reducing sensory feedback, making it difficult for patients to detect and respond to injuries. Diabetes-induced damage to neurotrophic factors and increased neuronal apoptosis result in diminished sensory perception. This diminished sensory feedback increases the risk of ulceration and highlights the need for interventions aimed at nerve protection and regeneration. Addressing neuropathy can aid in early injury detection and potentially prevent the development of DFUs [26,51].

Infection and trauma play central roles in the pathogenesis and progression of DFUs [52]. Peripheral neuropathy, a common complication of diabetes, reduces protective sensation and leads to repetitive microtrauma from ill-fitting footwear or unnoticed injuries. Structural deformities and limited joint mobility further exacerbate pressure points on the plantar surface, fostering ulcer formation. Once the protective skin barrier is breached, bacterial colonization can quickly escalate to infection. Infections not only impede wound healing through local inflammation and biofilm formation but also contribute to systemic complications. Severe infections can lead to cellulitis, abscess formation, and osteomyelitis, significantly increasing the risk of lower limb amputation. A prompt, accurate assessment of both trauma and infection is therefore essential to prevent adverse outcomes. Preventive strategies, including patient education, routine foot care, and appropriate footwear, are integral to reducing the incidence and severity of DFU.

Serological markers provide valuable insights into the systemic conditions affecting DFUs. Elevated CRP and ESR are indicators of systemic inflammation and correlate with DFU severity and healing outcomes [27]. Monitoring these markers is essential for assessing the inflammatory burden and adjusting treatment plans accordingly. Glycemic markers, such as HbA1c, reflect long-term blood glucose control and are crucial in managing DFU risk. High HbA1c levels are directly linked to an increased risk of DFUs and poor healing outcomes, reinforcing the need for consistent glycemic management. Additionally, acute fluctuations in blood glucose can exacerbate ulcer development and impair healing, further underlining the importance of stable glucose control in DFU prevention and management.

A comprehensive evaluation of DFUs is crucial for effective management and prognosis. Several clinical scoring systems have been developed to standardize assessment [53]. The Wagner classification remains widely used, focusing primarily on ulcer depth and the presence of gangrene or osteomyelitis. Complementing this, the University of Texas wound classification system incorporates parameters such as infection and ischemia, offering a more detailed stratification. The SINBAD system (Site, Ischemia, Neuropathy, Bacterial infection, Area, and Depth) provides a simplified yet informative approach suitable for resource-limited settings. In addition to these clinical tools, recent advancements in diagnostic imaging, such as thermography, hyperspectral imaging, and MRI, enhance the detection of tissue damage and infection. Furthermore, research into biochemical markers and molecular signatures holds promise for early diagnosis and monitoring. Together, these tools support clinicians in making informed decisions and tailoring treatment strategies.

Omics technologies have revolutionized our understanding of DFUs by providing comprehensive insights into the molecular and cellular changes associated with the condition [54]. Genomic studies have identified genetic variations that influence susceptibility to DFUs, while transcriptomics reveals changes in gene expression related to inflammation and wound healing. Proteomics and metabolomics offer deeper insights into the protein and metabolic profiles associated with DFUs, uncovering biomarkers that reflect disease processes and guide targeted therapies. These technologies enable a more detailed understanding of DFU mechanisms and support the development of personalized treatment strategies that are tailored to the individual patient [55].

Effective management of DFUs involves a multifaceted strategy that targets both the underlying etiologies and the ulcer itself [52]. The initial step typically includes meticulous wound debridement to eliminate necrotic tissue, which is essential for preparing the wound bed and preventing infection. Infection control is also critical and may require systemic or topical antibiotics, depending on the severity and microbial profile. Pressure offloading, particularly using total contact casting, helps redistribute weight and minimize mechanical stress on the affected area. In parallel, maintaining strict glycemic control is fundamental to enhancing the body’s healing capacity. Beyond these standard measures, adjunctive therapies are being increasingly adopted to enhance outcomes. For instance, recombinant growth factors such as platelet-derived growth factor have been employed to stimulate tissue regeneration. Stem cell therapies and bioengineered skin substitutes offer additional regenerative potential, particularly in chronic or non-healing ulcers. Moreover, hyperbaric oxygen therapy has demonstrated effectiveness in improving tissue oxygenation, especially in ischemic or hypoxic wounds. Looking ahead, innovative treatments such as gene therapy and nanotechnology-based drug delivery systems are under active investigation. These emerging approaches hold promise for more targeted and efficient management of DFU. Ultimately, the most effective treatment requires an individualized, evidence-based plan tailored to the patient’s specific risk factors and wound characteristics.

In summary, the interplay of hyperglycemia, inflammation, oxidative stress, neuropathy, and serological markers shapes the development and progression of DFUs. A multifaceted approach integrating insights from mechanistic studies, serological profiles, and omics technologies is essential for advancing both prevention and treatment strategies. Understanding these factors in detail can lead to improved prognostic accuracy and more effective management, ultimately enhancing patient outcomes and reducing the burden of DFUs.

Acknowledgments

Figure was created in https://BioRender.com.

  1. Funding information: This work was supported by the National Natural Science Foundation of China Youth Fund Project (82205117); Postdoctoral Research Project of Henan Province (HN2024083); and Research Special Project of Henan Province Traditional Chinese Medicine Clinical Research Base (2022JDZX135).

  2. Author contributions: Jixue Wang: conceptualization, writing original draft, and writing review and editing; Xirui Yang: conceptualization, literature review, writing original draft, and writing review and editing; Tao Zhou: writing original draft and writing review and editing; Haitao Ma: writing review and editing; Xingxing Yuan: literature review and writing review and editing; Shuxun Yan: supervision and writing review and editing; all authors have read and approved the final manuscript.

  3. Conflict of interest: Authors state no conflict of interest.

  4. Data availability statement: Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

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Received: 2025-01-15
Revised: 2025-05-12
Accepted: 2025-05-28
Published Online: 2025-08-08

© 2025 the author(s), published by De Gruyter

This work is licensed under the Creative Commons Attribution 4.0 International License.

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https://doi.org/10.1515/biol-2025-1137
Schlagwörter für diesen Artikel
diabetic foot ulcers; risk factors; prognostic markers; wound healing
Creative Commons
BY 4.0

Artikel in diesem Heft

  1. Biomedical Sciences
  2. Mechanism of triptolide regulating proliferation and apoptosis of hepatoma cells by inhibiting JAK/STAT pathway
  3. Maslinic acid improves mitochondrial function and inhibits oxidative stress and autophagy in human gastric smooth muscle cells
  4. Comparative analysis of inflammatory biomarkers for the diagnosis of neonatal sepsis: IL-6, IL-8, SAA, CRP, and PCT
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  8. Preliminary analysis of the role of small hepatitis B surface proteins mutations in the pathogenesis of occult hepatitis B infection via the endoplasmic reticulum stress-induced UPR-ERAD pathway
  9. Efficacy of alginate-coated gold nanoparticles against antibiotics-resistant Staphylococcus and Streptococcus pathogens of acne origins
  10. Battling COVID-19 leveraging nanobiotechnology: Gold and silver nanoparticle–B-escin conjugates as SARS-CoV-2 inhibitors
  11. Neurodegenerative diseases and neuroinflammation-induced apoptosis
  12. Impact of fracture fixation surgery on cognitive function and the gut microbiota in mice with a history of stroke
  13. COLEC10: A potential tumor suppressor and prognostic biomarker in hepatocellular carcinoma through modulation of EMT and PI3K-AKT pathways
  14. High-temperature requirement serine protease A2 inhibitor UCF-101 ameliorates damaged neurons in traumatic brain-injured rats by the AMPK/NF-κB pathway
  15. SIK1 inhibits IL-1β-stimulated cartilage apoptosis and inflammation in vitro through the CRTC2/CREB1 signaling
  16. Rutin–chitooligosaccharide complex: Comprehensive evaluation of its anti-inflammatory and analgesic properties in vitro and in vivo
  17. Knockdown of Aurora kinase B alleviates high glucose-triggered trophoblast cells damage and inflammation during gestational diabetes
  18. Calcium-sensing receptors promoted Homer1 expression and osteogenic differentiation in bone marrow mesenchymal stem cells
  19. ABI3BP can inhibit the proliferation, invasion, and epithelial–mesenchymal transition of non-small-cell lung cancer cells
  20. Changes in blood glucose and metabolism in hyperuricemia mice
  21. Rapid detection of the GJB2 c.235delC mutation based on CRISPR-Cas13a combined with lateral flow dipstick
  22. IL-11 promotes Ang II-induced autophagy inhibition and mitochondrial dysfunction in atrial fibroblasts
  23. Short-chain fatty acid attenuates intestinal inflammation by regulation of gut microbial composition in antibiotic-associated diarrhea
  24. Application of metagenomic next-generation sequencing in the diagnosis of pathogens in patients with diabetes complicated by community-acquired pneumonia
  25. NAT10 promotes radiotherapy resistance in non-small cell lung cancer by regulating KPNB1-mediated PD-L1 nuclear translocation
  26. Phytol-mixed micelles alleviate dexamethasone-induced osteoporosis in zebrafish: Activation of the MMP3–OPN–MAPK pathway-mediating bone remodeling
  27. Association between TGF-β1 and β-catenin expression in the vaginal wall of patients with pelvic organ prolapse
  28. Primary pleomorphic liposarcoma involving bilateral ovaries: Case report and literature review
  29. Effects of de novo donor-specific Class I and II antibodies on graft outcomes after liver transplantation: A pilot cohort study
  30. Sleep architecture in Alzheimer’s disease continuum: The deep sleep question
  31. Ephedra fragilis plant extract: A groundbreaking corrosion inhibitor for mild steel in acidic environments – electrochemical, EDX, DFT, and Monte Carlo studies
  32. Langerhans cell histiocytosis in an adult patient with upper jaw and pulmonary involvement: A case report
  33. Inhibition of mast cell activation by Jaranol-targeted Pirin ameliorates allergic responses in mouse allergic rhinitis
  34. Aeromonas veronii-induced septic arthritis of the hip in a child with acute lymphoblastic leukemia
  35. Clusterin activates the heat shock response via the PI3K/Akt pathway to protect cardiomyocytes from high-temperature-induced apoptosis
  36. Research progress on fecal microbiota transplantation in tumor prevention and treatment
  37. Low-pressure exposure influences the development of HAPE
  38. Stigmasterol alleviates endplate chondrocyte degeneration through inducing mitophagy by enhancing PINK1 mRNA acetylation via the ESR1/NAT10 axis
  39. AKAP12, mediated by transcription factor 21, inhibits cell proliferation, metastasis, and glycolysis in lung squamous cell carcinoma
  40. Association between PAX9 or MSX1 gene polymorphism and tooth agenesis risk: A meta-analysis
  41. A case of bloodstream infection caused by Neisseria gonorrhoeae
  42. Case of nasopharyngeal tuberculosis complicated with cervical lymph node and pulmonary tuberculosis
  43. p-Cymene inhibits pro-fibrotic and inflammatory mediators to prevent hepatic dysfunction
  44. GFPT2 promotes paclitaxel resistance in epithelial ovarian cancer cells via activating NF-κB signaling pathway
  45. Transfer RNA-derived fragment tRF-36 modulates varicose vein progression via human vascular smooth muscle cell Notch signaling
  46. RTA-408 attenuates the hepatic ischemia reperfusion injury in mice possibly by activating the Nrf2/HO-1 signaling pathway
  47. Decreased serum TIMP4 levels in patients with rheumatoid arthritis
  48. Sirt1 protects lupus nephritis by inhibiting the NLRP3 signaling pathway in human glomerular mesangial cells
  49. Sodium butyrate aids brain injury repair in neonatal rats
  50. Interaction of MTHFR polymorphism with PAX1 methylation in cervical cancer
  51. Convallatoxin inhibits proliferation and angiogenesis of glioma cells via regulating JAK/STAT3 pathway
  52. The effect of the PKR inhibitor, 2-aminopurine, on the replication of influenza A virus, and segment 8 mRNA splicing
  53. Effects of Ire1 gene on virulence and pathogenicity of Candida albicans
  54. Small cell lung cancer with small intestinal metastasis: Case report and literature review
  55. GRB14: A prognostic biomarker driving tumor progression in gastric cancer through the PI3K/AKT signaling pathway by interacting with COBLL1
  56. 15-Lipoxygenase-2 deficiency induces foam cell formation that can be restored by salidroside through the inhibition of arachidonic acid effects
  57. FTO alleviated the diabetic nephropathy progression by regulating the N6-methyladenosine levels of DACT1
  58. Clinical relevance of inflammatory markers in the evaluation of severity of ulcerative colitis: A retrospective study
  59. Zinc valproic acid complex promotes osteoblast differentiation and exhibits anti-osteoporotic potential
  60. Primary pulmonary synovial sarcoma in the bronchial cavity: A case report
  61. Metagenomic next-generation sequencing of alveolar lavage fluid improves the detection of pulmonary infection
  62. Uterine tumor resembling ovarian sex cord tumor with extensive rhabdoid differentiation: A case report
  63. Genomic analysis of a novel ST11(PR34365) Clostridioides difficile strain isolated from the human fecal of a CDI patient in Guizhou, China
  64. Effects of tiered cardiac rehabilitation on CRP, TNF-α, and physical endurance in older adults with coronary heart disease
  65. Changes in T-lymphocyte subpopulations in patients with colorectal cancer before and after acupoint catgut embedding acupuncture observation
  66. Modulating the tumor microenvironment: The role of traditional Chinese medicine in improving lung cancer treatment
  67. Alterations of metabolites related to microbiota–gut–brain axis in plasma of colon cancer, esophageal cancer, stomach cancer, and lung cancer patients
  68. Research on individualized drug sensitivity detection technology based on bio-3D printing technology for precision treatment of gastrointestinal stromal tumors
  69. CEBPB promotes ulcerative colitis-associated colorectal cancer by stimulating tumor growth and activating the NF-κB/STAT3 signaling pathway
  70. Oncolytic bacteria: A revolutionary approach to cancer therapy
  71. A de novo meningioma with rapid growth: A possible malignancy imposter?
  72. Diagnosis of secondary tuberculosis infection in an asymptomatic elderly with cancer using next-generation sequencing: Case report
  73. Hesperidin and its zinc(ii) complex enhance osteoblast differentiation and bone formation: In vitro and in vivo evaluations
  74. Research progress on the regulation of autophagy in cardiovascular diseases by chemokines
  75. Anti-arthritic, immunomodulatory, and inflammatory regulation by the benzimidazole derivative BMZ-AD: Insights from an FCA-induced rat model
  76. Immunoassay for pyruvate kinase M1/2 as an Alzheimer’s biomarker in CSF
  77. The role of HDAC11 in age-related hearing loss: Mechanisms and therapeutic implications
  78. Evaluation and application analysis of animal models of PIPNP based on data mining
  79. Therapeutic approaches for liver fibrosis/cirrhosis by targeting pyroptosis
  80. Fabrication of zinc oxide nanoparticles using Ruellia tuberosa leaf extract induces apoptosis through P53 and STAT3 signalling pathways in prostate cancer cells
  81. Haplo-hematopoietic stem cell transplantation and immunoradiotherapy for severe aplastic anemia complicated with nasopharyngeal carcinoma: A case report
  82. Modulation of the KEAP1-NRF2 pathway by Erianin: A novel approach to reduce psoriasiform inflammation and inflammatory signaling
  83. The expression of epidermal growth factor receptor 2 and its relationship with tumor-infiltrating lymphocytes and clinical pathological features in breast cancer patients
  84. Innovations in MALDI-TOF Mass Spectrometry: Bridging modern diagnostics and historical insights
  85. BAP1 complexes with YY1 and RBBP7 and its downstream targets in ccRCC cells
  86. Hypereosinophilic syndrome with elevated IgG4 and T-cell clonality: A report of two cases
  87. Electroacupuncture alleviates sciatic nerve injury in sciatica rats by regulating BDNF and NGF levels, myelin sheath degradation, and autophagy
  88. Polydatin prevents cholesterol gallstone formation by regulating cholesterol metabolism via PPAR-γ signaling
  89. RNF144A and RNF144B: Important molecules for health
  90. Analysis of the detection rate and related factors of thyroid nodules in the healthy population
  91. Artesunate inhibits hepatocellular carcinoma cell migration and invasion through OGA-mediated O-GlcNAcylation of ZEB1
  92. Endovascular management of post-pancreatectomy hemorrhage caused by a hepatic artery pseudoaneurysm: Case report and review of the literature
  93. Efficacy and safety of anti-PD-1/PD-L1 antibodies in patients with relapsed refractory diffuse large B-cell lymphoma: A meta-analysis
  94. SATB2 promotes humeral fracture healing in rats by activating the PI3K/AKT pathway
  95. Overexpression of the ferroptosis-related gene, NFS1, corresponds to gastric cancer growth and tumor immune infiltration
  96. Understanding risk factors and prognosis in diabetic foot ulcers
  97. Atractylenolide I alleviates the experimental allergic response in mice by suppressing TLR4/NF-kB/NLRP3 signalling
  98. FBXO31 inhibits the stemness characteristics of CD147 (+) melanoma stem cells
  99. Immune molecule diagnostics in colorectal cancer: CCL2 and CXCL11
  100. Inhibiting CXCR6 promotes senescence of activated hepatic stellate cells with limited proinflammatory SASP to attenuate hepatic fibrosis
  101. Cadmium toxicity, health risk and its remediation using low-cost biochar adsorbents
  102. Pulmonary cryptococcosis with headache as the first presentation: A case report
  103. Solitary pulmonary metastasis with cystic airspaces in colon cancer: A rare case report
  104. RUNX1 promotes denervation-induced muscle atrophy by activating the JUNB/NF-κB pathway and driving M1 macrophage polarization
  105. Morphometric analysis and immunobiological investigation of Indigofera oblongifolia on the infected lung with Plasmodium chabaudi
  106. The NuA4/TIP60 histone-modifying complex and Hr78 modulate the Lobe2 mutant eye phenotype
  107. Experimental study on salmon demineralized bone matrix loaded with recombinant human bone morphogenetic protein-2: In vitro and in vivo study
  108. A case of IgA nephropathy treated with a combination of telitacicept and half-dose glucocorticoids
  109. Analgesic and toxicological evaluation of cannabidiol-rich Moroccan Cannabis sativa L. (Khardala variety) extract: Evidence from an in vivo and in silico study
  110. Wound healing and signaling pathways
  111. Combination of immunotherapy and whole-brain radiotherapy on prognosis of patients with multiple brain metastases: A retrospective cohort study
  112. To explore the relationship between endometrial hyperemia and polycystic ovary syndrome
  113. Research progress on the impact of curcumin on immune responses in breast cancer
  114. Biogenic Cu/Ni nanotherapeutics from Descurainia sophia (L.) Webb ex Prantl seeds for the treatment of lung cancer
  115. Dapagliflozin attenuates atrial fibrosis via the HMGB1/RAGE pathway in atrial fibrillation rats
  116. Glycitein alleviates inflammation and apoptosis in keratinocytes via ROS-associated PI3K–Akt signalling pathway
  117. ADH5 inhibits proliferation but promotes EMT in non-small cell lung cancer cell through activating Smad2/Smad3
  118. Apoptotic efficacies of AgNPs formulated by Syzygium aromaticum leaf extract on 32D-FLT3-ITD human leukemia cell line with PI3K/AKT/mTOR signaling pathway
  119. Novel cuproptosis-related genes C1QBP and PFKP identified as prognostic and therapeutic targets in lung adenocarcinoma
  120. Bee venom promotes exosome secretion and alters miRNA cargo in T cells
  121. Treatment of pure red cell aplasia in a chronic kidney disease patient with roxadustat: A case report
  122. Comparative bioinformatics analysis of the Wnt pathway in breast cancer: Selection of novel biomarker panels associated with ER status
  123. Kynurenine facilitates renal cell carcinoma progression by suppressing M2 macrophage pyroptosis through inhibition of CASP1 cleavage
  124. RFX5 promotes the growth, motility, and inhibits apoptosis of gastric adenocarcinoma cells through the SIRT1/AMPK axis
  125. ALKBH5 exacerbates early cardiac damage after radiotherapy for breast cancer via m6A demethylation of TLR4
  126. Phytochemicals of Roman chamomile: Antioxidant, anti-aging, and whitening activities of distillation residues
  127. Circadian gene Cry1 inhibits the tumorigenicity of hepatocellular carcinoma by the BAX/BCL2-mediated apoptosis pathway
  128. The TNFR-RIPK1/RIPK3 signalling pathway mediates the effect of lanthanum on necroptosis of nerve cells
  129. Longitudinal monitoring of autoantibody dynamics in patients with early-stage non-small-cell lung cancer undergoing surgery
  130. The potential role of rutin, a flavonoid, in the management of cancer through modulation of cell signaling pathways
  131. Construction of pectinase gene engineering microbe and its application in tobacco sheets
  132. Construction of a microbial abundance prognostic scoring model based on intratumoral microbial data for predicting the prognosis of lung squamous cell carcinoma
  133. Sepsis complicated by haemophagocytic lymphohistiocytosis triggered by methicillin-resistant Staphylococcus aureus and human herpesvirus 8 in an immunocompromised elderly patient: A case report
  134. Sarcopenia in liver transplantation: A comprehensive bibliometric study of current research trends and future directions
  135. Advances in cancer immunotherapy and future directions in personalized medicine
  136. Can coronavirus disease 2019 affect male fertility or cause spontaneous abortion? A two-sample Mendelian randomization analysis
  137. Heat stroke associated with novel leukaemia inhibitory factor receptor gene variant in a Chinese infant
  138. PSME2 exacerbates ulcerative colitis by disrupting intestinal barrier function and promoting autophagy-dependent inflammation
  139. Hyperosmolar hyperglycemic state with severe hypernatremia coexisting with central diabetes insipidus: A case report and literature review
  140. Efficacy and mechanism of escin in improving the tissue microenvironment of blood vessel walls via anti-inflammatory and anticoagulant effects: Implications for clinical practice
  141. Merkel cell carcinoma: Clinicopathological analysis of three patients and literature review
  142. Ecology and Environmental Science
  143. Optimization and comparative study of Bacillus consortia for cellulolytic potential and cellulase enzyme activity
  144. The complete mitochondrial genome analysis of Haemaphysalis hystricis Supino, 1897 (Ixodida: Ixodidae) and its phylogenetic implications
  145. Epidemiological characteristics and risk factors analysis of multidrug-resistant tuberculosis among tuberculosis population in Huzhou City, Eastern China
  146. Indices of human impacts on landscapes: How do they reflect the proportions of natural habitats?
  147. Genetic analysis of the Siberian flying squirrel population in the northern Changbai Mountains, Northeast China: Insights into population status and conservation
  148. Diversity and environmental drivers of Suillus communities in Pinus sylvestris var. mongolica forests of Inner Mongolia
  149. Global assessment of the fate of nitrogen deposition in forest ecosystems: Insights from 15N tracer studies
  150. Fungal and bacterial pathogenic co-infections mainly lead to the assembly of microbial community in tobacco stems
  151. Influencing of coal industry related airborne particulate matter on ocular surface tear film injury and inflammatory factor expression in Sprague-Dawley rats
  152. Temperature-dependent development, predation, and life table of Sphaerophoria macrogaster (Thomson) (Diptera: Syrphidae) feeding on Myzus persicae (Sulzer) (Homoptera: Aphididae)
  153. Eleonora’s falcon trophic interactions with insects within its breeding range: A systematic review
  154. Agriculture
  155. Integrated analysis of transcriptome, sRNAome, and degradome involved in the drought-response of maize Zhengdan958
  156. Variation in flower frost tolerance among seven apple cultivars and transcriptome response patterns in two contrastingly frost-tolerant selected cultivars
  157. Heritability of durable resistance to stripe rust in bread wheat (Triticum aestivum L.)
  158. Molecular mechanism of follicular development in laying hens based on the regulation of water metabolism
  159. Animal Science
  160. Effect of sex ratio on the life history traits of an important invasive species, Spodoptera frugiperda
  161. Plant Sciences
  162. Hairpin in a haystack: In silico identification and characterization of plant-conserved microRNA in Rafflesiaceae
  163. Widely targeted metabolomics of different tissues in Rubus corchorifolius
  164. The complete chloroplast genome of Gerbera piloselloides (L.) Cass., 1820 (Carduoideae, Asteraceae) and its phylogenetic analysis
  165. Field trial to correlate mineral solubilization activity of Pseudomonas aeruginosa and biochemical content of groundnut plants
  166. Correlation analysis between semen routine parameters and sperm DNA fragmentation index in patients with semen non-liquefaction: A retrospective study
  167. Plasticity of the anatomical traits of Rhododendron L. (Ericaceae) leaves and its implications in adaptation to the plateau environment
  168. Effects of Piriformospora indica and arbuscular mycorrhizal fungus on growth and physiology of Moringa oleifera under low-temperature stress
  169. Effects of different sources of potassium fertiliser on yield, fruit quality and nutrient absorption in “Harward” kiwifruit (Actinidia deliciosa)
  170. Comparative efficiency and residue levels of spraying programs against powdery mildew in grape varieties
  171. The DREB7 transcription factor enhances salt tolerance in soybean plants under salt stress
  172. Using plant electrical signals of water hyacinth (Eichhornia crassipes) for water pollution monitoring
  173. Food Science
  174. Phytochemical analysis of Stachys iva: Discovering the optimal extract conditions and its bioactive compounds
  175. Review on role of honey in disease prevention and treatment through modulation of biological activities
  176. Computational analysis of polymorphic residues in maltose and maltotriose transporters of a wild Saccharomyces cerevisiae strain
  177. Optimization of phenolic compound extraction from Tunisian squash by-products: A sustainable approach for antioxidant and antibacterial applications
  178. Liupao tea aqueous extract alleviates dextran sulfate sodium-induced ulcerative colitis in rats by modulating the gut microbiota
  179. Toxicological qualities and detoxification trends of fruit by-products for valorization: A review
  180. Polyphenolic spectrum of cornelian cherry fruits and their health-promoting effect
  181. Optimizing the encapsulation of the refined extract of squash peels for functional food applications: A sustainable approach to reduce food waste
  182. Advancements in curcuminoid formulations: An update on bioavailability enhancement strategies curcuminoid bioavailability and formulations
  183. Impact of saline sprouting on antioxidant properties and bioactive compounds in chia seeds
  184. The dilemma of food genetics and improvement
  185. Bioengineering and Biotechnology
  186. Impact of hyaluronic acid-modified hafnium metalorganic frameworks containing rhynchophylline on Alzheimer’s disease
  187. Emerging patterns in nanoparticle-based therapeutic approaches for rheumatoid arthritis: A comprehensive bibliometric and visual analysis spanning two decades
  188. Application of CRISPR/Cas gene editing for infectious disease control in poultry
  189. Preparation of hafnium nitride-coated titanium implants by magnetron sputtering technology and evaluation of their antibacterial properties and biocompatibility
  190. Preparation and characterization of lemongrass oil nanoemulsion: Antimicrobial, antibiofilm, antioxidant, and anticancer activities
  191. Corrigendum
  192. Corrigendum to “Utilization of convolutional neural networks to analyze microscopic images for high-throughput screening of mesenchymal stem cells”
  193. Corrigendum to “Effects of Ire1 gene on virulence and pathogenicity of Candida albicans”
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© 2025 De Gruyter Brill
Heruntergeladen am 16.11.2025 von https://www.degruyterbrill.com/document/doi/10.1515/biol-2025-1137/html
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