Ischemia-reperfusion injury (IRI) is a pathophysiological process occurring after blood supply restoration to tissues or organs, causing unexpected cellular damage. It involves multiple complex mechanisms, but inflammation and oxidative stress are the main causes. IRI can damage vital organs such as the heart, brain, liver, and kidneys, affecting patient prognosis and quality of life. Therefore, the prevention and treatment of IRI have become a key area in clinical and basic research. Prussian blue, a metal-organic framework material, is approved by the U.S. Food and Drug Administration for treating heavy metal poisoning. In 2016, research indicated that Prussian blue nanoparticles had multi-enzyme activities like catalase, peroxidase, and superoxide dismutase, enabling them to scavenge reactive oxygen species and combat inflammation, establishing them as a highly promising nanozyme. Leveraging their unique antioxidative and anti-inflammatory properties, Prussian blue nanozyme (PBNZ) can directly target key pathological pathways of IRI. Furthermore, PBNZ can serve as efficient drug delivery systems, and through functional modifications, they enable the targeted delivery of therapeutic agents, thereby synergistically enhancing treatment efficacy. Currently, PBNZ have demonstrated significant therapeutic potential in IRI models involving various organs and tissues such as the heart, brain, liver, kidneys, and skin flaps. This review aims to outline IRI's key pathological mechanisms, analyze how PBNZ combats oxidative stress and inflammation, and summarize its recent application advancements in treating IRI in different organs. The goal is to offer theoretical reference and research insights for the future development of novel nanozyme-based therapeutic strategies against IRI.

Atherosclerosis research has been significantly advanced by mouse models, particularly genetically engineered strains such as apolipoprotein E-deficient mice and low-density lipoprotein receptor-deficient mice (Ldlr<sup>-/-</sup>). These mouse models replicate the hyperlipidemia-driven plaque pathogenesis, providing critical insights into lipid metabolism, inflammation, and therapeutic responses. Classic models play an important role in validating the effects of lipid-lowering therapies such as statins and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors. There are also some limitations, including species-specific lipoprotein profiles and incomplete replication of advanced human plaque complexity. Novel models have emerged to address these gaps, incorporating features such as hemodynamic stress, humanized lipid metabolism, and inducible gene regulation to complement the inadequacies of classic models, thereby better simulating the multifactorial complexity of atherosclerosis. For example, adeno-associated virus serotype 8 carrying the Pcsk9[D377Y] mutant gene and Ldlr-antisense oligonucleotide mice integrate hemodynamic stress, humanized lipid metabolism, and multifactorial comorbidities. However, there are still some shortcomings, including metabolic disparities, inadequate modeling of plaque rupture/thrombosis, and oversimplification of systemic disease interactions. Future directions prioritize next-generation models featuring humanized lipoprotein profiles, dynamic gene regulation, and combined with metabolic syndrome features. These approaches can be synergized with advanced phenotyping tools—including single-cell omics and intravital imaging—alongside artificial intelligence-driven multi-omics integration. By bridging translational gaps between murine pathophysiology and human disease complexity, these mouse models promise to accelerate the development of atherosclerosis therapies.

Aim: To evaluate the long-term impact of obstructive sleep apnea (OSA) risk profile on atrial fibrillation (AF) recurrence after catheter ablation in patients with paroxysmal AF. Methods: This prospective study enrolled 161 patients with paroxysmal AF undergoing initial ablation. Patients were stratified by the Berlin Questionnaire (BQ) into high-risk (n = 94) and low-risk (n = 67) OSA groups. Atrial tachyarrhythmias occurring within the initial three months were defined as early recurrence, whereas recurrence beyond three months was defined as late recurrence. A subgroup of 71 patients with recurrence underwent a redo ablation. Results: After 16.1 ± 0.4 years, multivariable models revealed that a BQ-defined high OSA risk was independently associated with early recurrence (odds ratio [OR] 1.99, 95% confidence interval [CI] 1.02-3.86, P = 0.043), whereas it was not independently associated with late recurrence after the initial procedure (hazard ratio [HR] 1.05, 95%CI: 0.70-1.57, P = 0.810). Cox regression identified early recurrence (HR 2.95, 95%CI: 1.99-4.39, P < 0.001) and baseline high-sensitivity C-reactive protein (hs-CRP; HR 1.02, 95%CI: 1.00-1.03, P = 0.022) as independent predictors of late recurrence after the initial procedure. Following redo ablation, early recurrence remained a strong independent predictor (HR 5.93, 95%CI: 2.13-16.50, P < 0.001). Conclusions: The BQ-defined high OSA risk was an independent predictor of early recurrence; however, it was not significantly associated with late recurrence after AF ablation. Early recurrence was the strongest predictor of long-term outcome, highlighting the importance of management during the post-procedural blanking period.

The integrity of the vascular endothelium is fundamental to its barrier function, maintaining vascular homeostasis and microenvironmental stability, and serves as a prerequisite for preventing certain vascular diseases. After vascular integrity is compromised, endothelial progenitor cells (EPCs), a diverse population of progenitor cells with the capacity to develop into endothelial cells, can reconstruct blood vessels. This occurs primarily through two mechanisms: (1) direct integration into existing vessels for repair; and (2) paracrine secretion of proangiogenic factors to promote EPC mobilization and migration, regulate immune functions, and inhibit endothelial hyperplasia. This review aims to elucidate the mechanisms by which EPCs participate in vascular remodeling, and to discuss the latest advances in clinical translation strategies such as cell therapy, EPC-derived exosome therapy, and EPC functional modulation, as well as the current challenges in standardization and clinical application.

Aim: Cardiovascular-kidney-metabolic (CKM) syndrome accelerates aging and increases mortality. We evaluated whether Triglyceride-Glucose-Waist-to-Height Ratio (TyG-WHtR), a marker of insulin resistance, predicts mortality in CKM and whether age acceleration mediates this association. Methods: This investigation enrolled 16,145 individuals diagnosed with CKM syndrome. The relationships between TyG-WHtR and mortality were examined using multivariable Cox proportional hazards models, threshold effect analysis, and restricted cubic splines. Besides, the mediating role of age acceleration was investigated through mediation analysis. Risk within different populations was assessed using interaction tests and subgroup analysis. Results: In multivariate Cox proportional hazards analyses, TyG-WHtR showed a positive association with mortality outcomes. Per one standard deviation (1-SD) increase, the hazard of cardiovascular death was 18% higher (hazard ratio (HR): 1.180; 95% confidence interval (CI): 1.08-1.29), while all-cause mortality risk rose by 8.6% (HR: 1.086, 95%CI: 1.01-1.17). Both cardiovascular and all-cause mortality showed a strong U-shaped association with TyG-WHtR. Mediation analysis revealed that PhenoAge acceleration and Klemera-Doubal Method age acceleration mediated 19.7% and 15.8% of the association between TyG-WHtR and all-cause mortality, respectively, and 20.7% and 16.8% of the association between TyG-WHtR and cardiovascular mortality, respectively. Conclusion: TyG-WHtR is associated with mortality in patients with CKM syndrome, partly through accelerated aging. It is positively associated with age acceleration and exhibits a U-shaped relationship with mortality. Targeting the metabolic-aging crosstalk may help reduce mortality in CKM patients.

Panvascular aging-related diseases, including coronary artery disease, ischemic stroke, and peripheral artery disease, are leading global causes of death and disability, yet their management remains fragmented. Emerging technologies offer solutions to this challenge. Big data integration across imaging, multi-omics, wearables, and environmental exposures provides opportunities for cross-organ insights but faces issues of heterogeneity and privacy. Artificial intelligence enables early detection and refined risk prediction by recognizing subtle vascular changes and integrating biomarkers, though adoption is limited by interpretability and bias. Foundation models, through cross-modal learning, offer a unifying framework for mechanism discovery, personalized management, and digital twin applications. By linking technological innovation with clinical practice, these approaches can transform panvascular aging management and promote healthy longevity. Importantly, translating these innovations into policy and practice will be essential for advancing equitable vascular health and achieving population-level impact.

We read with great interest a recent study investigating the role of nuclear receptor coactivator 7 (NCOA7) as a critical regulator of lysosomal function, oxysterol, and bile acid metabolism, and its link to endothelial cells (ECs) inflammation and immune activation in pulmonary artery hypertension (PAH). The study demonstrated that NCOA7 deficiency exacerbated lysosomal dysfunction, leading to inflammatory sterol accumulation and immune activation, which subsequently triggers endothelial immune responses. Translationally, NCOA7 activation emerges as a promising therapeutic strategy, while plasma oxysterol and bile acid levels offer potential prognostic biomarkers for PAH severity and mortality.

In this special interview, Professor Barry A. Franklin shared key experiential and research-based insights on professional success, exercise-based cardiovascular therapy, and the impactful role of cardiorespiratory fitness in promoting long-term health outcomes. (a) Professional success is built on clearly defined written goals, consistent daily action, personal responsibility, a mindset of happiness, optimism, and gratitude, and exemplary service to others; (b) Outstanding academic and clinical careers require effective mentorship, strong communication skills, advanced training and continuing education, disciplined work habits, and proactive management of stress and health; (c) Aerobic and resistance training provide complementary benefits in combating cardiovascular disease, with aerobic exercise contributing most strongly to long-term survival; (d) Cardiorespiratory fitness or VO2max (maximum volume of oxygen uptake), expressed as metabolic equivalents (METs), is a powerful, independent, and additive predictor of survival, with each 1-MET (one metabolic equivalent) increase associated with a mortality reduction of ~ 15%-17%; (e) Higher fitness levels significantly reduce the risk and improve the prognosis of heart failure with preserved ejection fraction and heart failure with reduced ejection fraction, independent of body mass index and traditional risk factors; (f) Although aerobic fitness declines rapidly with detraining, it is reversible, while muscle strength can be largely maintained with one resistance training session per week; (g) To date, no pharmacologic therapy can elicit the increases in metabolism needed to improve fitness, as well as the associated favorable adaptations, and safe, accessible activities such as stair climbing and daily walking provide substantial cardiovascular risk reduction.

Endovascular recanalization has revolutionized the treatment of peripheral artery disease (PAD), offering minimally invasive alternatives to open surgery. However, permanent metallic stents, while effective in restoring blood flow, are associated with long-term complications such as chronic inflammation, restenosis, and stent thrombosis. Bioresorbable scaffolds (BRS) have emerged as an innovative solution, providing temporary mechanical support while delivering antiproliferative drugs before fully degrading, thus eliminating the risks associated with permanent implants. Significant advancements in bioresorbable materials have led to the development of new-generation scaffolds with improved radial strength, controlled degradation rates, and enhanced drug-eluting properties. Several BRS platforms, including polymer- and magnesium-based designs, are undergoing clinical and preclinical evaluation for peripheral applications. Early trials suggest that BRS may offer comparable short-term patency rates to conventional stents while potentially reducing late adverse events. However, challenges such as scaffold thrombosis, mechanical integrity in large and calcified vessels, and long-term efficacy remain under investigation. This narrative review explores the evolution of BRS technology, the mechanisms of scaffold resorption, current clinical evidence, and future prospects for their use in peripheral endovascular interventions. As research progresses, BRS may represent a paradigm shift in the treatment of PAD, offering a balance between structural support and vascular restoration.

Pan-vascular diseases comprise a spectrum of atherosclerosis-driven vascular disorders that involve multiple vital organs, including the heart, brain, kidneys, and peripheral circulation. Despite being distributed across different clinical specialties due to increasing medical subspecialization, conditions such as coronary artery disease, ischemic stroke, and peripheral artery disease are interconnected manifestations of a unified, systemic vascular pathology. This conceptual shift highlights the need to consider these disorders within an integrated pan-vascular framework rather than as isolated clinical entities. Inflammation is a central driver in pan-vascular pathogenesis, accelerating atherosclerosis and increasing cardiovascular event risk. In the inflammatory cascade of pan-vascular diseases, chemokines play a pivotal role as regulators, facilitating the recruitment and activation of immune cells. C-C motif chemokine ligand 17 (CCL17) is essential for T cell development in the thymus. It binds to the C-C chemokine receptor 4 (CCR4) and exhibits chemotactic activity towards T lymphocytes, mainly T helper 2 (Th2) cells and regulatory T cells. This review summarizes the biological properties of CCL17, its mechanistic roles in pan-vascular pathologies, and its clinical translational potential as a biomarker and therapeutic target.