Liu Q, Wang YF, Geng Y, Zhang P, Lv TT. Cardiovascular aging as a modifiable biological process: Mechanisms, clinical phenotypes, and translational opportunities. World J Cardiol 2026; 18(8): 124876 [DOI: 10.4330/wjc.124876]
Corresponding Author of This Article
Ting-Ting Lv, MD, Associate Research Scientist, Department of Cardiology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, No. 168 Litang Road, Changping District, Beijing 102218, China. lvtingting0616@163.com
Research Domain of This Article
Cardiac & Cardiovascular Systems
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review-article
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Liu Q, Wang YF, Geng Y, Zhang P, Lv TT. Cardiovascular aging as a modifiable biological process: Mechanisms, clinical phenotypes, and translational opportunities. World J Cardiol 2026; 18(8): 124876 [DOI: 10.4330/wjc.124876]
Qing Liu, Department of General Practice, Suining Central Hospital, Suining 629000, Sichuan Province, China
Yi-Fei Wang, Yu Geng, Ping Zhang, Ting-Ting Lv, Department of Cardiology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing 102218, China
Author contributions: Liu Q conceived the review, wrote the manuscript, and drew all figures using FigDraw; Wang YF analyzed and interpreted key findings, revised the manuscript for important intellectual content; Geng Y analyzed and interpreted key findings, reviewed the manuscript for accuracy and consistency; Zhang P conceived the project vision, and revised the manuscript for scientific coherence and impact; Lv TT designed the research scope and objectives, supervised the interpretation of critical findings, and revised the manuscript for structural and intellectual rigor.
AI contribution statement: The author(s) declared that generative AI was not used in the creation of this manuscript.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Corresponding author: Ting-Ting Lv, MD, Associate Research Scientist, Department of Cardiology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, No. 168 Litang Road, Changping District, Beijing 102218, China. lvtingting0616@163.com
Received: June 26, 2026 Revised: July 13, 2026 Accepted: August 20, 2026 Published online: August 26, 2026 Processing time: 61 Days and 24 Hours
Abstract
Cardiovascular aging, a primary driver of the increasing prevalence of cardiovascular disease in older adults, involves a complex biological basis beyond mere chronological age. From a geroscience perspective, aging is now understood as a dynamic and potentially modifiable process, believed to be governed by interconnected molecular hallmarks such as cellular senescence, mitochondrial dysfunction, epigenetic remodeling, telomere attrition, and impaired proteostasis. This review synthesizes recent advancements in aging biology, illustrating how these core hallmarks appear to converge on major cardiovascular phenotypes including atherosclerosis, heart failure with preserved ejection fraction, hypertension, and arrhythmia through shared mechanisms. These mechanisms encompass endothelial dysfunction, vascular smooth muscle cell phenotypic switching, myocardial fibrosis, chronic inflammation, and electrophysiological instability. We also summarize current approaches to assessing cardiovascular aging, which include imaging-based indices, circulating biomarkers, and emerging epigenetic clocks capable of quantifying biological age and age acceleration. At the interventional level, growing preclinical and early-phase clinical evidence suggests that geroprotective strategies show promise for altering cardiovascular aging trajectories. These strategies include lifestyle modification, metabolic regulation, senotherapeutics, and modulation of mechanistic target of rapamycin and nicotinamide adenine dinucleotide pathways. Nevertheless, significant challenges persist, such as the absence of standardized aging assessment frameworks, uncertainties regarding long-term safety, and the necessity for rigorously designed clinical trials with aging-related endpoints. By connecting the molecular hallmarks of aging with clinically measurable cardiovascular phenotypes and novel therapeutic strategies, this review underscores cardiovascular aging as a clinically tractable and translationally relevant model for transforming geroscience principles into actionable approaches for disease prevention and healthy longevity.
Core Tip: This review synthesizes current evidence that cardiovascular aging is driven by interconnected hallmarks: Cellular senescence, mitochondrial dysfunction, epigenetic remodeling, telomere attrition, and impaired proteostasis which converge on atherosclerosis, heart failure with preserved ejection fraction, hypertension, and arrhythmia. We highlight emerging assessment tools including imaging-based indices, circulating biomarkers, and epigenetic clocks for quantifying biological age, and critically evaluate geroprotective strategies ranging from lifestyle modification to senotherapeutics and nicotinamide adenine dinucleotide/mechanistic target of rapamycin modulation. Bridging geroscience principles with cardiovascular medicine, this review positions cardiovascular aging as a clinically modifiable target for promoting healthy longevity.
