Mesenchymal stem-cell-derived exosomes (MSC-sEVs) represent a promising cell-free strategy for myocardial repair. Building upon the recent work by Bashir et al., we propose a complementary metabolic-lipid framework in which specific phospholipid cargoes allosterically regulate glucose-6-phosphate dehydrogenase (G6PD) to enhance pentose-phosphate-pathway (PPP) activity and sustain NADPH-dependent redox balance. Observations from LVAD-supported myocardium reveal coordinated up-regulation of G6PD-PPP enzymes during reverse remodeling, linking metabolic reprogramming to structural recovery. Lipid-mediated modulation of G6PD may therefore provide a pharmacologic bridge between exosome-based paracrine signaling and redox-driven myocardial regeneration, advancing metabolism-guided therapeutic design in heart failure.

Abdominal aortic aneurysm (AAA) is a chronic aortic disease that currently lacks effective pharmacological treatments. Growth Differentiation Factor 11 (GDF11) is a member of transforming growth factor β (TGF-β) superfamily associated with cardiovascular diseases. Transcriptomic analysis of GSE57691 revealed significantly reduced GDF11 expression in AAA tissues, with further decline from early- to advanced-stage disease. GDF11 levels correlated negatively with IL-1β, IL-6, MMP-2, and MMP-9, and positively with ACTA2 and TGF-β/Smad2/3 signaling. In an Ang II-induced AAA model of ApoE mice, GDF11 was markedly decreased, accompanied by inflammation, matrix degradation, and vascular remodeling. AAV-mediated GDF11 overexpression improved survival, reduced AAA incidence, limited aortic dilation, and attenuated elastin degradation and collagen deposition. Mechanistically, GDF11 inhibited inflammatory cytokines, downregulated MMP-2/9, restored ACTA2, and modulated TGF-β/Smad2/3 signaling. In vitro, GDF11 attenuated Ang II-induced phenotypic switching of vascular smooth muscle cells (VSMCs), while inhibition of TGF-β/Smad2/3 signaling reversed these effects. In conclusion, GDF11 mitigates AAA progression by suppressing inflammation, preserving extracellular matrix integrity, and maintaining VSMC phenotype via TGF-β/Smad2/3 signaling, highlighting its potential as a therapeutic target for AAA.

Emerging lipid-lowering therapies, such as Plozasiran, target apolipoprotein C-III (APOC-III) by inhibiting its hepatic production at the mRNA level, presenting a novel approach to lipid regulation. However, the safety and efficacy of plozasiran have yet to be fully established.

While reperfusion is essential for restoring blood flow, it can paradoxically exacerbate myocardial injury by disrupting energy metabolism, leading to cell necrosis, apoptosis, and structural damage. Despite the significance of ischemia-reperfusion (I/R) injury, effective treatments remain scarce, highlighting the need for a deeper understanding of its underlying mechanisms to develop targeted therapies.

Anemia is common among women undergoing elective percutaneous coronary intervention (PCI), yet remains under-addressed in contemporary ACC/AHA guidelines. We evaluated the association between baseline anemia and short- and long-term outcomes after PCI.

Disseminated intravascular coagulation (DIC) is a life-threatening condition characterized by uncontrolled coagulation and systemic inflammation, often triggered by sepsis. Recent studies highlight the role of N6-methyladenosine (m6A) modification in regulating endothelial dysfunction and coagulation pathways. However, the specific role of Wilms tumor 1-associated protein (WTAP)-a component of the m6A methyltransferase complex-in sepsis-induced DIC remains poorly understood.

this study aims to screen Protease-activated receptor 1 (PAR1) inhibitory active components with low bleeding side effects from anti-thrombin phytochemicals in Polygonum amplexicaule D. Don var. sinense Forb (PAF) to achieve multi-pathway antithrombosis without disrupting platelet hemostasis.

Mineralocorticoid receptor antagonists (MRAs) improve outcomes in patients with heart failure with preserved ejection fraction (HFpEF), yet comparative effectiveness between steroidal and nonsteroidal agents remains unknown. Our aim was to compare cardiovascular and safety outcomes associated with finerenone versus spironolactone among patients with HFpEF.

Atherosclerotic stenosis is a progressive vascular disease characterized by vascular narrowing. Bone marrow mesenchymal stem cell-derived extracellular vesicles (BMSC-EVs) have been reported to alleviate endothelial cell dysfunction.

Pulmonary hypertension (PH) is a clinicopathological syndrome characterized by structural and functional alterations in the pulmonary vasculature arising from heterogeneous etiologies (including hypoxia) and diverse pathogenic mechanisms. These changes elevate pulmonary vascular resistance and increase pulmonary arterial pressure, ultimately progressing to right heart failure and potential fatality. Resistin-like molecule (RELM)-β activates multiple signaling pathways. This study aimed to explore the role of RELM-β in the development of chronic hypoxia-induced PH and its potential mechanisms.

We appreciate the thoughtful commentary by Drs. Dziewierz and Siudak regarding our study comparing tirzepatide versus semaglutide in post-CABG diabetic patients. While we acknowledge the inherent limitations of observational research, our propensity score matching achieved near-perfect balance across 40+ covariates (SMD = 0.033), including comprehensive medication proxies for diabetes control, lipid management, and blood pressure control. We observed consistent protective effects across multiple distinct outcome domains-cerebrovascular, cardiovascular, thrombotic, mortality, and healthcare utilization-with nine outcomes significant after Benjamini-Hochberg correction. The cerebrovascular benefit is particularly noteworthy given semaglutide's neutral stroke effect in SELECT trial, suggesting differential GIP receptor-mediated neurovascular protection. SURPASS-CVOT, comparing tirzepatide to dulaglutide (not semaglutide) in general ASCVD populations, addresses a different clinical question and may lack power for post-CABG subgroup analysis. Our findings provide hypothesis-generating evidence for an understudied high-risk population, warranting further investigation in dedicated trials.

Venous thromboembolism (VTE), encompassing deep vein thrombosis and pulmonary embolism, constitutes a significant cause of postoperative morbidity and mortality among surgical patients. Despite the widespread use of low-molecular-weight heparin (LMWH) for thromboprophylaxis, conventional fixed-dose regimens frequently yield subprophylactic anti-factor Xa (anti-Xa) levels, particularly in individuals with obesity, renal impairment, or altered drug pharmacokinetics. These interindividual variations in LMWH pharmacodynamics underscore the need for personalized anticoagulant strategies. Anti-Xa-guided dosing has emerged as a strategy to individualize prophylaxis and optimize outcomes.

Lipoprotein(a) [Lp(a)] is increasingly recognized as a genetically determined, independent risk factor for atherosclerotic cardiovascular disease (ASCVD). This review examines the structure, pathophysiology, and epidemiology of Lp(a), with a focus on its contribution to ASCVD and related conditions such as aortic valve stenosis and peripheral artery disease. The main research question addresses how Lp(a) influences cardiovascular risk and how emerging therapies may modify this risk.

Kawasaki disease (KD) is an acute systemic vasculitis causing coronary artery lesions (CAL). Paeoniflorin (PF) exerts anti-inflammatory and antioxidant properties, but its role in KD remains unclear. This study aims to elucidate the effects of PF on CAL and the underlying regulatory mechanisms.

The study by Kimoto et al. investigated the relationship between metabolic syndrome (MetS) and breast cancer incidence in a large Japanese cohort exceeding one million women, revealing an unexpected age-dependent pattern. Both pre-MetS and MetS were associated with a lower incidence of breast cancer, particularly in women younger than 50 years, whereas this association attenuated or reversed after 60 years of age. In our correspondence, we discuss potential biological and methodological explanations for this paradox. We highlight the importance of heterogeneity in MetS definitions (Japanese vs. modified ATP III), the role of menopausal status beyond chronological age, and possible confounding by screening behavior and competing cardiovascular mortality. While the authors' interpretation involving anovulatory cycles and adipose-derived estrogen provides a plausible mechanistic framework, we emphasize the need for analyses stratified by actual menopausal status, repeated measures of MetS components, and competing-risk modeling. Overall, the findings underscore the complex, age-modulated interaction between metabolic dysregulation and breast carcinogenesis, reinforcing the necessity of menopause-specific risk assessment and standardized MetS definitions in future research.