Aging is a major independent risk factor for cardiovascular disease (CVD), the leading cause of death worldwide, particularly in older adults [1,2]. With global population aging, the burden of age-related CVDs—such as heart failure (HF), atherosclerosis, arrhythmias, and vascular dysfunction—is projected to rise, emphasizing the need to understand aging’s biological drivers [3–5]. Cellular senescence, a state of permanent cell cycle arrest triggered by stressors like DNA damage, telomere shortening, and oxidative stress, is central to aging and related diseases.
