Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, with its prevalence rising sharply with age [1,2]. Cellular senescence has emerged as a pivotal contributor to the pathophysiology of CVD, offering novel insights into potential therapeutic interventions [3–5]. Initially described as a protective mechanism to prevent the proliferation of damaged cells (Fig. 1) [6], cellular senescence is now recognized for its deleterious effects in tissues, particularly in the cardiovascular system [7–9].
