Objective. Advanced glycation end products (AGEs) are featured metabolites associated with diabetic cardiomyopathy which is characterized by heart failure caused by myocyte apoptosis. Selenium was proved cardioprotective. This study was aimed at investigating the therapeutic effects and underlying mechanisms of selenium supplementation on AGE‐induced heart failure. Methods. Rats and primary myocytes were exposed to AGEs. Selenium supplementation was administrated. Cardiac functions and myocyte apoptosis were evaluated. Oxidative stress was assessed by total antioxidant capacity (TAC), reactive oxygen species (ROS) generation, and GPX activity. Expression levels of DNA methyltransferases (DNMTs) and glutathione peroxidase 1 (GPX1) were evaluated. DNA methylation of the GPX1 promoter was analyzed. Results. AGE exposure elevated intracellular ROS generation, induced myocyte apoptosis, and impaired cardiac functions. AGE exposure increased DNMT1 and DNMT2 expression, leading to the reduction of GPX1 expression and activity in the heart. Selenium supplementation decreased DNMT2 expression, recovered GPX1 expression and activity, and alleviated intracellular ROS generation and myocyte apoptosis, resulting in cardiac function recovery. DNA methylation analysis in primary myocytes indicated that selenium supplementation or DNMT inhibitor AZA treatment reduced DNA methylation of the GPX1 gene promoter. Selenium supplementation and AZA administration showed synergic inhibitory effect on GPX1 gene promoter methylation. Conclusions. Selenium supplementation showed cardioprotective effects on AGE‐induced heart failure by suppressing ROS‐mediated myocyte apoptosis. Selenium supplementation suppressed ROS generation by increasing GPX1 expression via inhibiting DNMT2‐induced GPX1 gene promoter DNA methylation in myocytes exposed to AGEs.

This current study aimed to investigate the relationship between the triglyceride-glucose (TyG) index and in-hospital all-cause mortality of coronary artery disease (CAD) in patients with different glucose metabolic statuses. Participants were divided into three groups according to tertiles of the TyG index. Glucose metabolic status was classified as normal glucose regulation, pre-diabetes mellitus, and diabetes mellitus (DM). The primary outcome was in hospital all-cause mortality. We observed a significant relationship between the TyG index and in-hospital deaths of patients with CAD in this study. After adjusting for multiple factors in the logistic regression model, the TyG index was still an independent risk factor, and the T3 group (OR, 2.311; 95% CI = 1.237–4.317; P = 0.009) was correlated with a 2.311-fold risk compared with the T1 group. In the subgroup analysis of different glucose metabolic status, the T3 group (OR, 1.541; 95% CI: 1.013–2.344; P = 0.043) were associated with a significantly higher risk of in-hospital deaths in CAD patients with DM. An increased TyG index was correlated with a higher risk of in-hospital all-cause mortality. Our study indicated that TyG index could be a valuable predictor of in-hospital death of CAD patients, especially for individuals with DM.

Background: The atherogenic index of plasma (AIP), calculated from triglyceride and high-density lipoprotein cholesterol levels, is associated with atherosclerosis and coronary artery disease (CAD). However, evidence concerning the impact of the AIP on CAD severity remains limited. This study aims to assess the correlation between AIP and the severity of CAD. Methods: This study included 19,929 hospitalized participants diagnosed with CAD. After excluding participants with missing data, aged >75 years, or diagnosed with chronic kidney disease or cancer, a total of 2561 individuals were included. The 2561 participants were divided into three AIP tertile groups: AIP1 (AIP <0.016, n = 854), AIP2 (0.016 ≤ AIP < 0.216, n = 853), and AIP3 (AIP ≥0.216, n = 854). In this study, CAD severity was determined by the count of coronary arteries exhibiting stenosis of 50% or greater. Multivessel CAD was defined as ≥50% stenosis in two or more major coronary arteries. The relationship between AIP and CAD severity was assessed using logistic regression models. Results: Results indicate that the AIP independently predicts CAD severity, with an odds ratio of 1.700 (95% confidence interval (CI): 1.160–2.491; p = 0.007). The AIP3 group demonstrated a significantly higher risk of multivessel CAD compared to the AIP1 group (odds ratio (OR), 1.441; 95% CI: 1.124–1.848; p = 0.004), particularly in patients without diabetes mellitus (OR, 1.421; 95% CI: 1.030–1.962; p = 0.033). Conclusions: The AIP was significantly associated with CAD severity, suggesting that it could be a convenient and valuable marker for severity stratification in patients with CAD in clinical practice.

Objective: Heart failure is a complex end stage result of various cardiovascular diseases, and has a poor prognosis. Exercise training according to oxidative stress, myocardial fibrosis, inflammation pathways improve cardiac function. The aim of this study was to investigate the possible protective effects of exercise training against cardiac damage in doxorubicin (DOX)-induced heart failure in Sprague-Dawley Rats. Design and method: This study used 45 male Sprague-Dawley (SD) rats weighing 150 ± 20 g that were randomly divided into a control group (normal saline), doxorubicin (DOX) group and DOX plus exercise (DOX + E) group. Heart failure was induced experimentally by intraperitoneal injections of the cardiotoxic agent DOX. All groups received different treatment for 8 weeks. Blood samples were obtained from the inferior vena cava and collected in serum tubes; the blood samples were stored at minus 80°C until use. Heart tissues were fixed in 10% formalin and then embedded in paraffin for histological evaluation. The heart was stored in liquid nitrogen for immunoblotting or mRNA analysis. Results: Left ventricular fractional shortening and ejection fraction were higher in DOX + E group rats than in DOX group rats on an echocardiographic examination (Figure 1 and Table 1). Significant cardiac tissue damage (haematoxylin and eosin, Masson's trichrome staining) was seen in rats of the DOX group compared to those of the DOX + E group (Figure2). Exercise inhibited DOX-induced cardiac fibrosis (transforming growth factor, smooth muscle actin, collagen I, and collagen III) and oxidative stress (Nox4, p53) in an immunoblotting analysis (Figure 3 and 4). Conclusions: These results indicate that exercise training may be a potential therapeutic target for cardiac damage caused by DOX-induced heart failure.