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
Article-Type of This Article
review-article
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
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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
Core Tip
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.
