Stress-induced hyperglycemia (SIH) is a physiological response to acute or chronic stress characterized by elevated blood glucose levels. It is prevalent in both patients with and without diabetes, particularly those with acute or critical illnesses. The development of SIH is characterized by complex interactions among catecholamines, cortisol, and inflammatory mediators such as cytokines, resulting in increased hepatic glucose production and insulin resistance. While mild to moderate SIH may provide a protective mechanism during stress, prolonged or excessive hyperglycemia can exacerbate inflammation and oxidative stress, contributing to adverse outcomes in conditions such as acute myocardial infarction, heart failure, and cerebrovascular diseases. The stress-hyperglycemia ratio (SHR), defined as the ratio of admission glucose to estimated mean glucose (derived from glycated hemoglobin [HbA1c]), has emerged as a valuable tool for quantifying stress hyperglycemia. Unlike absolute glucose levels, the SHR accounts for background hyperglycemia and provides a more accurate indicator of the relative glucose elevation associated with critical illness. Extensive research has demonstrated a U-shaped or J-shaped relationship of the SHR with disease outcomes, indicating that both low and high SHRs are associated with increased mortality and morbidity. The SHR has shown significant predictive value in cardiovascular diseases (e.g., acute coronary syndrome, heart failure), cerebrovascular diseases (e.g., acute ischemic stroke, intracerebral hemorrhage), and infectious diseases (e.g., sepsis, pneumonia). It also plays a role in other conditions, such as acute pancreatitis and certain cancers. The ease of calculating the SHR from widely available admission glucose and HbA1c tests makes it a practical and valuable prognostic marker in clinical settings. This review examines the relationship between the SHR and critical illnesses, highlighting its mechanisms and predictive value across various diseases. Predictive value of SHR in cardiovascular, cerebrovascular, infectious, and other diseases.

Diabetic cardiomyopathy is a myocardial structural and functional abnormality directly caused by diabetes and is a principal factor in the development of cardiovascular complications in patients with diabetes. The study aims to investigate the role of circOGDH in the development of DCM and elucidate its precise underlying mechanisms. We established two well-characterized diabetic mouse models, C57BL/6J and db/db, and assessed cardiac function by serum lactate dehydrogenase activity assay and echocardiography, as well as quantitative histological analyses of the extent of myocardial fibrosis in combination with HE staining and Masson trichrome staining. The results demonstrated that there was a significant upregulation of circOGDH expression levels in myocardial tissues of mice in a diabetic state, accompanied by the increased expression of key effector proteins of PANoptosis. It is noteworthy that the knockdown of circOGDH led to a substantial enhancement in cardiac function indices, a reduction in the area of myocardial fibrosis, and the effective inhibition of the PANoptosis process in myocardial tissues. In the H9c2 cells model, silencing of circOGDH also exhibited significant protective effects, including increased cell survival, reduced levels of oxidative stress, decreased apoptosis, and suppressed expression of PANoptosis-related proteins. Subsequent employing RNA pull-down, RNA immunoprecipitation, and co-immunoprecipitation experimental methods have elucidated, for the first time, the molecular mechanism by which circOGDH specifically targets and regulates RIPK3 through the HMGB1 signaling pathway. The present study definitively demonstrated that upregulation of circOGDH expression in a diabetic state could exacerbate pathological damage in DCM by activating the HMGB1-RIPK3 signaling pathway.

Objective: The primary objective of this study was to assess the diagnostic potential of galectin-3 (Gal-3), fractalkine (FKN), interleukin (IL)-6, microRNA(miR)-21, and cardiac troponin I (cTnI) in patients with ischemic cardiomyopathy (ICM). Method: A total of 78 ICM patients (Case group) and 80 healthy volunteers (Control group) admitted to our hospital for treatment or physical examination from Aug. 2018 to Feb. 2020 were included in the current study. The serum concentration of Gal-3, FKN, IL-6, miR-21, and plasma expression of cTnI of both groups were determined. The severity of ICM was classified using New York Heart Association (NYHA) scale. Results: When compared with the control group, the case group had a significantly high blood concentration of Gal-3, FKN, IL-6, miR-21, and cTnI (P < 0.001). NYHA class II patients had lower blood levels of Gal-3, FKN, IL-6, miR-21, and cTnI than that in patients of NYHA class III and IV without statistical significance (P > 0.05). However, statistical significance could be achieved when comparing the above-analyzed markers in patients classified between class III and IV. Correlation analysis also revealed that serum levels of Gal-3, FKN, IL-6, miR-21, and cTnI were positively correlated with NYHA classification (R = 0.564, 0.621, 0.792, 0.981, P < 0.05). Conclusion: Our study revealed that up-regulated serum Gal-3, FKN, IL-6, miR-21, and cTnI levels were closely related to the progression of ICM. This association implies that these biomarkers have diagnostic potential, offering a promising avenue for early detection and monitoring of ICM progression.

Atherosclerosis (AS) is a prevalent cardiovascular disease, and emerging evidence highlights the critical role of gut microbiota in its development. Trimethylamine‐N‐oxide (TMAO), a metabolite derived from gut microbiota, is thought to promote AS progression by regulating smooth muscle protein 22‐alpha (SM22α)‐mediated inflammation in vascular smooth muscle cells. This study aims to explore the molecular mechanisms of TMAO in AS through multi‐omics analysis, particularly its effects on SIRT1 inhibition and SM22α modulation. 16S ribosomal RNA sequencing revealed an altered gut microbiota composition in AS mice, characterized by increased Bacteroides and decreased Firmicutes. Metabolomics analysis indicated elevated levels of TMAO in AS mice. Transcriptomic data and cell experiments further confirmed that TMAO promotes AS by regulating SM22α‐mediated inflammation via SIRT1 regulation. These findings suggest that TMAO accelerates progression through the SIRT1 and SM22α‐related pathways, offering novel therapeutic targets for AS intervention.

Purpose This meta-analysis aimed to evaluate the efficacy and safety of non-vitamin K antagonist oral anticoagulants (NOACs) compared with vitamin K antagonists (VKAs) in patients with atrial fibrillation (AF) and type 2 valvular heart disease (VHD). Methods We searched the PubMed, LILACS, and MEDLINE databases to retrieve, randomized controlled trials (RCTs) comparing NOACs and VKAs in patients with AF and type 2 VHD, excluding mitral stenosis (moderate to severe, of rheumatic origin) or mechanical heart valves. The efficacy outcomes assessed were stroke and systemic embolism (SE), while safety outcomes included major bleeding and intracranial hemorrhage (ICH). Results Seven RCTs, including 16,070 patients with AF and type 2 VHD, were included. NOACs reduced the risk of stroke/SE (relative risk [RR], 0.75; 95% confidence interval [CI], 0.64–0.89; P = 0.0005), with no significant difference in major bleeding (RR, 0.88; 95% CI, 0.64–1.21; P = 0.43). The risk of ICH was reduced with NOACs (RR, 0.46; 95% CI, 0.27–0.77; P = 0.003). For patients with AF and bioprosthetic heart valve (five trials, 2805 patients), stroke/SE risks (RR, 0.65, 95% CI, 0.44–0.96) with NOACs were superior to VKAs. Major bleeding risks without ENVISAGE TAVI AF trial (RR, 0.53; 95% CI, 0.30–0.94; P = 0.03) with NOACs were superior to VKAs. The risks of ICH (RR, 0.61; 95% CI 0.34–1.09; P = 0.09) with NOACs were comparable to VKAs. Conclusions NOACs demonstrate efficacy and safety in patients with AF and type 2 VHD and reduce the risk of stroke/SE and ICH when compared with those with VKAs.

The lymphatic system is the same reticular fluid system as the circulatory system found throughout the body in vascularized tissues. Lymphatic vessels are low-pressure, blind-ended tubular structures that play a crucial role in maintaining tissue fluid homeostasis, immune cell transport, and lipid absorption. The heart also has an extensive lymphatic network, and as research on cardiac lymphatics has progressed in recent years, more and more studies have found that cardiac lymphangiogenesis may ameliorate certain cardiovascular diseases, and therefore stimulation of cardiac lymphangiogenesis may be an important tool in the future treatment of cardiovascular diseases. This article briefly reviews the development and function of cardiac lymphatic vessels, the interaction of cardiac lymphatic vessels with cardiovascular diseases (including atrial fibrillation, coronary atherosclerosis, and heart failure), and finally discusses the therapeutic potential of targeted cardiac lymphatic therapy for cardiovascular diseases.