Increasing evidences have indicated that there are gender differences in the prevalence of metabolic syndrome(MS), but the mechanism is uncertain. A total of 711 subjects aged 35–65 years accepted health examinations both in 1992 and 2007. Since 114 subjects had MS and 7 had heart disease at baseline, they were excluded from the analysis. Therefore, 590 subjects with complete data (male: 61.5 %) were available and analysed. After the relationship between gender and incident MS at follow-up was tested, these subjects were categorized into four groups according to the baseline resting heart rate(RHR) classified by genders. Trend tests of MS incidences across the four groups of resting heart rate were conducted by Cochran-Armitage tend tests in both men and women. Additionally, three logistic regression models were used to estimate the effects of RHR on the new onset of MS by taking RHR as a continuous variable(per 4 beats/min elevation). Gender(women) itself was an independent risk factor for incident MS at follow-up(OR = 2.64, 1.33–5.23, P = 0.005). The incidences of MS according to the RHR categories showed a statistical linear trend in women(P for trend = 0.018) rather than in men(P for trend = 0.194). The ORs[95 % confidence intervals(CIs)] of MS for each 4 bpm elevation in RHR was 1.18(1.03–1.36)(P = 0.020) in a univariate model, 1.20 (1.04–1.38) (P = 0.011) adjusted for age and health related behaviors only and 1.23(1.06–1.43)(P = 0.007) adjusted for age, health related behaviors and pre-existing components of MS in the baseline in women. Otherwise, RHR did not have any significant associations with incident MS in men neither in a univariate model nor in multivariate models. In this study, elevated RHR is correlated with the development of MS in women rather than in men.

Diabetic cardiomyopathy (DCM) is a severe cardiovascular complication of diabetes characterized by myocardial hypertrophy, fibrosis, and impaired cardiac function. Fibroblast growth factor 21 (FGF21) has emerged as a promising therapeutic target due to its antifibrotic, antioxidant, and anti-inflammatory properties. Our commentary summarizes and affirms the recent study by Wang et al., which demonstrates the significant role of ferroptosis in DCM pathogenesis. FGF21 has shown promise as a therapeutic target for DCM, potentially inhibiting ferroptosis, mitigating oxidative damage, and protecting cardiomyocyte function. Mechanistically, the study identified ATF4 as an upstream regulator of FGF21 in DCM, revealing that FGF21 directly interacts with ferritin and extends its half-life, thus inhibiting ferroptosis in DCM. These findings provide a theoretical basis for understanding the pathogenesis and treatment of DCM. Our commentary suggests that future studies should explore the role of non-cardiomyocyte cell types in DCM, verify findings with clinical samples, and address comprehensive methods for ferroptosis detection. Additionally, we discuss the clinical application and future potential of FGF21-based therapies for DCM. Such efforts may contribute to advancing DCM diagnosis and treatment, fostering the development of innovative therapeutic strategies.

Introduction: We aimed to explore the prognostic value of the aspartate aminotransferase to alanine aminotransferase (AST/ALT) ratio in non-surgical patients with type 2 diabetes hospitalized for heart failure.Material and methods: Using a large electronic medical record-based cohort of diabetes in China (WECODe), we gathered data on non-surgical hospitalized patients with type 2 diabetes and heart failure from 2011 to 2019. Baseline AST/ALT ratio was calculated. The primary outcomes were all-cause death within 30 days after discharge, composite cardiac events, major acute kidney injury, and major systemic infection. A multivariable Cox proportional regression model was utilized to evaluate the association between the AST/ALT ratio and outcomes.Results: This retrospective cohort included 8,073 patients (39.4% women) with type 2 diabetes hospitalized for heart failure. The median age was 71 years. Higher AST/ALT ratio was associated with higher risks of poor endpoints (with per standard deviation increment in AST/ALT ratio, for death within 30 days after discharge: adjusted hazard ratio [HR], 1.35, 95% confidence interval [CI], 1.21 to 1.50; for composite cardiac events: HR, 1.18, 95% CI: 1.06 to 1.31). Compared to patients in the lowest quartile for the AST/ALT ratio, those in the highest quartile have elevated risk of death within 30 days after discharge and major systemic infection (HRs [95% CIs]: 1.61 [1.18 to 2.19] and 1.28 [1.06 to 1.56], respectively). Subgroup analyses and sensitivity analyses confirmed the robustness of the findings.Conclusions: Type 2 diabetes patients hospitalized for heart failure with the AST/ALT ratio in the highest quartile face a poor short-term prognosis.

Primary aldosteronism (PA) is the most frequent form of secondary endocrine hypertension, which is characterized by excessive aldosterone secretion and suppressed renin. The currently recommended diagnostic algorithm is very clear, and the plasma aldosterone-to-renin ratio (ARR) is considered the first-line screening test. However, this indicator is influenced by many factors, some of which may cause false-negative results, consequently leading to underdiagnosed PA. Here, we report the rare case of a 38-year-old man who presented with bilateral accessory renal arteries and aldosterone-producing adenoma but had a negative ARR test result.

Introduction Hypertension constitutes the primary health burden of cardiovascular diseases, and the global control of blood pressure (BP) remains insufficient. Single pill combinations (SPCs) are employed as a means to streamline the management of poor BP control due to non-adherence and treatment inertia. The compound reserpine and triamterene tablets constitute a quadruple SPC, comprising reserpine 0.1 mg, dihydralazine 12.5 mg, hydrochlorothiazide 12.5 mg and triamterene 12.5 mg. It is widely employed in primary medical institutions and has favourable efficacy, tolerability and cost-effectiveness. Methods and analysis The COSPQ-BP trial is a 12-week prospective randomised controlled trial to enrol 1332 patients with primary mild-to-moderate hypertension. Participants who meet the inclusion criteria will be randomly assigned to a 1:1 ratio to an intervention group (compound reserpine and triamterene tablets) or a control group (valsartan/hydrochlorothiazide). The primary outcome will be mean changes from baseline in 24-hour ambulatory systolic BP after intervention for 12 weeks. The secondary outcomes have been predetermined and will primarily encompass the following: (1) changes in other BP measures, as well as changes in blood lipids, blood glucose and uric acid at 12 weeks and (2) evaluation of the impact of starting antihypertensive therapy with compound reserpine and triamterene tablets or valsartan/hydrochlorothiazide on the depressive and anxiety statess of patients. Ethics and dissemination The study protocol (version number: V5.0, version date: 17 January 2023) has been approved by the ethics committee (Biomedical Ethics Committee of West China Hospital of Sichuan University, approval number: Review (51) in 2023). Written informed consent will be obtained from each participant by researchers. The findings of this study will be disseminated through conference presentations and peer-reviewed publications. Trial registration This study was registered at the Chinese Clinical Trials Registry (ChiCTR2300067920). The COSPQ-BP trial is currently enrolling. The study period will be from 1 January 2024 to 31 December 2025.

Age-related diseases such as cardiovascular disorders, neurodegeneration, and metabolic syndrome share a unifying pathological signature—persistent low-grade inflammation or “inflammaging”. Among the transcriptional regulators that orchestrate this process, RUNX1 has emerged as a pivotal molecular hub linking inflammation, cellular senescence, and tissue dysfunction. Traditionally recognized for its role in hematopoietic lineage specification, RUNX1 is now known to exert context-dependent regulatory functions across diverse organ systems. Its activation in aged tissues is driven by convergent pro-inflammatory and stress-related pathways—including NF-κB, MAPK, JAK/STAT, and oxidative signaling—that reinforce RUNX1 transcriptional activity through epigenetic reprogramming and chromatin remodeling. Sustained RUNX1 upregulation contributes to cellular senescence, fibrotic remodeling, and regenerative blockade, forming a self-perpetuating cycle of “inflammation amplification–functional decline”. In the cardiovascular, nervous, and hematopoietic systems, aberrant RUNX1 activation underlies fibrosis, neuroinflammation, and clonal hematopoiesis, respectively, establishing RUNX1 as a shared driver of age-associated pathology. The isoform-specific and temporally dynamic regulation of RUNX1 underpins its dual pro- and anti-inflammatory roles, highlighting its translational potential as both a biomarker and therapeutic target. A range of emerging intervention strategies has demonstrated promising capacity to precisely modulate RUNX1 activity. Collectively, these advances position RUNX1 at the intersection of inflammation, epigenetic instability, and tissue degeneration, opening new avenues for targeted intervention in inflammaging and age-related diseases.