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Background The cold winter weather in northern China influences the dietary habits of its residents, contributing to a heightened risk of cardiovascular disorders, such as hypertension and coronary heart disease. Key factors include low vegetable consumption and high salt and fat intakes. This study aims to investigate the relationships between northern dietary nutrient intake in northern China and cardiovascular disorders during the winter season. Methods A food frequency questionnaire tailored to the actual eating habits in northern China was designed. Retrospective data from 955 Chinese adults were collected from November to March between 2014 to 2023. Logistic regression was employed to analyze the relationship between dietary nutrients and cardiovascular diseases, with model performance assessed using receiver operating characteristic (ROC) curves. Results Adjusted for gender, age, and body mass index (BMI), an inverse association was observed between vitamin A ( OR = 0.706, 95% CI: 0.550, 0.907), nicotinic acid ( OR = 0.584, 95% CI: 0.447, 0.762), phosphorus ( OR = 0.777, 95% CI: 0.608, 0.994), selenium ( OR = 0.719, 95% CI: 0.560, 0.923), zinc ( OR = 0.683, 95% CI: 0.531, 0.880), methionine ( OR = 0.730, 95% CI: 0.569, 0.936), arginine ( OR = 0.753, 95% CI: 0.588, 0.964), lysine ( OR = 0.706, 95% CI: 0.550, 0.907), aspartic acid ( OR = 0.730, 95% CI: 0.569, 0.936) and hypertension. Additionally, a negative association was found between niacin ( OR = 0.752, 95% CI: 0.597, 0.946) and coronary heart disease. Conversely, a positive association was identified between iodine and hypertension ( OR = 1.305, 95% CI: 1.020, 1.669) and coronary heart disease ( OR = 1.301, 95% CI: 1.037, 1.634). Conclusion Our study suggests that maintaining a balanced dietary intake of vitamin A, niacin, phosphorus, selenium, zinc, methionine, arginine, lysine, and aspartic acid can be beneficial in preventing hypertension. Adequate niacin intake is associated with a lower risk of coronary heart disease. However, excessive iodine intake may contribute to hypertension and coronary heart disease.

Background Nonalcoholic fatty liver disease (NAFLD) is a chronic condition characterized by a progressive decline in liver function, leading to disruptions in liver integrity and metabolic function, resulting in lipid deposition and excessive accumulation of extracellular matrix (ECM). The pathogenesis of NAFLD is complex and not yet fully understood, contributing to the absence of specific therapeutic strategies. Peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-activated transcription factor pivotal in regulating lipid and glucose metabolism. However, the impacts of PPARγ on NAFLD remains insufficiently explored. Thus, this study aimed to investigate the role of PPARγ in NAFLD and its underlying molecular mechanisms. Methods Chemical detection kits were utilized to quantify collagen content, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) level variations. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to assess alterations in extracellular matrix-related genes and inflammatory response genes in liver tissue and HepG2 cells, while western blotting was conducted to analyze the levels of both PPARγ and the TGF-β/Smad signaling pathway. Results Our findings unveiled significantly reduced PPARγ expression in a rat model of NAFLD, leading to subsequent activation of the TGF-β/Smad signaling pathway. Furthermore, PPARγ activation effectively mitigated NAFLD progression by inhibiting inflammation and fibrosis-related gene expression and collagen production. On a cellular level, PPARγ activation was found to inhibit the expression of extracellular matrix-related genes such as matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9), along with inflammatory response genes interleukin (IL)-1β and IL-6. Additionally, PPARγ activation led to a significant decrease in the levels of ALT and AST. At the molecular level, PPARγ notably down-regulated the TGF-β/Smad signaling pathway, which is known to promote liver fibrosis. Conclusion These groundbreaking findings underscore PPARγ activation as a promising therapeutic approach to delay NAFLD progression by targeting the TGF-β/Smad signaling pathway in hepatic cells. This highlights the potential of PPARγ as a promising therapeutic target for NAFLD management in clinical settings.

Objective This study aimed to estimate the incidence rate and clinical characteristics of inflammatory bowel disease (IBD) in the Chinese population, specially comparing the North and South regions. Methods We designed a questionnaire survey for patients diagnosed with IBD and conducted a systematic literature search in PubMed, China National Knowledge Internet, and Wanfang digital database, covering studies published between 2012 and 2022. Meta-analysis was performed to determine the overall incidence rate and prevalence of clinical manifestations of Crohn’s disease (CD) and ulcerative colitis (UC) in mainland China. Clinical phenotypes and demographic characteristics were calculated with 95% confidence intervals (CI). A comparison between the northern and southern regions was also conducted. Results The questionnaire survey included 440 patients, and 64 publications were included for Meta-analysis. The overall incidence rates of IBD, CD, and UC were 1.36 (95% CI: 0.79-2.33) per 100,000 person-years, 0.23 (95% CI: 0.09-0.58) per 100,000 person-years, and 1.12 (95% CI: 0.69-1.80) per 100,000 person-years, respectively. The incidence rates of IBD, CD, and UC were all higher in southern China compared to the North. Clinical characteristics of 440 IBD patients from the questionnaire and 2,821 CD patients and 12,809 UC patients from the literature were analyzed. There were more male patients compared to female patients. CD cases in the North exhibited earlier disease diagnosis ( P < 0.01), more upper gastrointestinal lesions ( P < 0.01), and higher hospitalizations rates ( P < 0.01) compared to the South. UC cases in the North had higher severity ( P < 0.01), anemia rates ( P < 0.01), and weight loss ( P < 0.01) compared to the South. Conclusions The incidence rates of IBD, CD, and UC were higher in southern China than in the North. Northern patients exhibited more severe symptoms compared to their southern counterparts.

Objective Myocardial ischemia-reperfusion injury (MIRI) is one of the leading causes of death from cardiovascular disease in humans, especially in individuals exposed to cold environments. Long non-coding RNAs (lncRNAs) regulate MIRI through multiple mechanisms.This study explored the regulatory effect of lncRNA-AK138945 on myocardial ischemia-reperfusion injury and its mechanism. Methods In vivo , 8- to 12-weeks-old C57BL/6 male mice underwent ligation of the left anterior descending coronary artery for 50 minutes followed by reperfusion for 48 hours. In vitro , the primary cultured neonatal mouse ventricular cardiomyocytes (NMVCs) were treated with 100 μmol/L hydrogen peroxide (H 2 O 2 ). The knockdown of lncRNA-AK138945 was evaluated to detect cardiomyocyte apoptosis, and a glucose-regulated, endoplasmic reticulum stress-related protein 94 (GRP94) inhibitor was used to detect myocardial injury. Results We found that the expression level of lncRNA-AK138945 was reduced in MIRI mouse heart tissue and H 2 O 2 -treated cardiomyocytes. Moreover, the proportion of apoptosis in cardiomyocytes increased after lncRNA-AK138945 was silenced. The expression level of Bcl2 protein was decreased, and the expression level of Bad, Caspase 9 and Caspase 3 protein was increased. Our further study found that miR-1a-3p is a direct target of lncRNA-AK138945, after lncRNA-AK138945 was silenced in cardiomyocytes, the expression level of miR-1a-3p was increased while the expression level of its downstream protein GRP94 was decreased. Interestingly, treatment with a GRP94 inhibitor (PU-WS13) intensified H 2 O 2 -induced cardiomyocyte apoptosis. After overexpression of FOXO3, the expression levels of lncRNA-AK138945 and GRP94 were increased, while the expression levels of miR-1a-3p were decreased. Conclusion LncRNA-AK138945 inhibits GRP94 expression by regulating miR-1a-3p, leading to cardiomyocyte apoptosis. The transcription factor Forkhead Box Protein O3 (FOXO3) participates in cardiomyocyte apoptosis induced by endoplasmic reticulum stress through up-regulation of lncRNA-AK138945.

Background and Objective Cardiac fibrosis is a pathological reparative process that follows myocardial infarctionand is associated with compromised cardiac systolic and reduced cardiac compliance. The Wnt signaling pathway is closely implicated in organ fibrosis, and Notum, a highly conserved secreted inhibitor, modulates Wnt signaling. The objective of this study was to explore the role and mechanism of Notum in cardiac fibrosis. Methods A mouse model of cardiac remodeling was established through left coronary artery ligation surgery, with the addition of Notum injection following myocardial infarction surgery. The protective effect of Notum on myocardial infarction was assessed by evaluating cardiac function, including survival rate, echocardiographic assessment, and cardiac contraction analyses. Inflammatory cell necrosis and infiltration were confirmed through H&E and Masson staining. The expression of fibrosis-related genes and β-catenin pathway markers was detected using Western blot quantificational RT-PCR (qRT-PCR). Additionally, EdU, wound healing, and immunofluorescence staining analyses were performed to detect the effect of Notum’s in transforming growth factor beta-1 (TGF-β1) induced myofibroblast transformation. Results The administration of Notum treatment resulted in enhanced survival rates, improved cardiac function, and decreased necrosis and infiltration of inflammatory cells in mice subjected to left coronary artery ligation. Furthermore, Notum effectively impeded the senescence of cardiac fibroblasts and hindered their pathological transformation into cardiac fibroblasts. Additionally, it significantly reduced collagen production and attenuated the activation of the Wnt/β-catenin pathway. Our preliminary investigations successfully demonstrated the therapeutic potential of Notum in both fibroblasts in vitro and in a mouse model of myocardial infarction-induced cardiac fibrosis in vivo . Conclusion Notum inhibition of the Wnt/β-catenin signaling pathway and cardiac fibroblast senescence ultimately hampers the onset of cardiac fibrosis. Our findings suggest that Notum could represent a new therapeutic strategy for the treatment of cardiac fibrosis.

Background Myocardial infarction (MI) is associated with higher morbidity and mortality in the world, especially in cold weather. YBX1 is an RNA-binding protein that is required for pathological growth of cardiomyocyte by regulating cell growth and protein synthesis. But YBX1, as an individual RNA-binding protein, regulates cardiomyocytes through signaling cascades during myocardial infarction remain largely unexplored. Methods In vivo, the mouse MI model was induced by ligating the left anterior descending coronary artery (LAD), and randomly divided into sham operation group, MI group, MI+ YBX1 knockdown/overexpression group and MI+ negative control (NC) group. The protective effect of YBX1 was verified by echocardiography and triphenyltetrazolium chloride staining. In vitro, mitochondrial-dependent apoptosis was investigated by using CCK8, TUNEL staining, reactive oxygen species (ROS) staining and JC-1 staining in hypoxic neonatal mouse cardiomyocytes (NMCMs). Results YBX1 expression of cardiomyocytes was downregulated in a mouse model and a cellular model on the ischemic condition. Compared to mice induced by MI, YBX1 overexpression mediated by adeno-associated virus serotype 9 (AAV9) vector reduced the infarcted size and improved cardiac function. Knockdown of endogenous YBX1 by shRNA partially aggravated ischemia-induced cardiac dysfunction. In hypoxic cardiomyocytes, YBX1 overexpression decreased lactic dehydrogenase (LDH) release, increased cell viability, and inhibited apoptosis by affecting the expression of apoptosis related proteins, while knockdown of endogenous YBX1 by siRNA had the opposite effect. Overexpression of YBX1 restored mitochondrial dysfunction in hypoxic NMCMs by increasing mitochondrial membrane potential and ATP content and decreasing ROS. In hypoxic NMCMs, YBX1 overexpression increased the expression of phosphorylated phosphatidylinositol 3 kinase (PI3K)/AKT, and the antiapoptosis effect of YBX1 was eliminated t by LY294002, PI3K/AKT inhibitor. Conclusion YBX1 protected the heart from ischemic damage by inhibiting the mitochondrial-dependent apoptosis through PI3K/AKT pathway. It is anticipated that YBX1 may serve as a novel therapeutic target for MI.