Aging is a significant risk factor for cardiovascular diseases, and cellular senescence plays a crucial role in this process. Senescence, characterized by irreversible cell cycle arrest and the manifestation of a senescence-associated secretory phenotype (SASP), contributes to the onset and progression of various cardiovascular diseases. Preclinical studies have shown that senolytic drugs effectively remove senescent cells in cardiac and vascular systems, offering potential therapeutic avenues for alleviating cardiovascular diseases. However, more preclinical investigations and clinical trials are needed to assess the safety and efficacy of senolytic treatments. The review highlights the detrimental impact of senescence on various cardiovascular diseases, including systemic atherosclerosis, hypertension, congestive heart failure, arrhythmias, and valvular heart diseases. It also discusses the beneficial effects of senolytics in reducing the burden of senescent cells and improving tissue function. Despite encouraging findings, several questions remain, such as the specific cell types targeted by senolytics and the precise mechanisms through which senescence hinders recovery after myocardial infarction and ischemia-reperfusion injury. Further research is essential to clarify these issues and advance the development of senolytic therapies for cardiovascular diseases.Aging is a significant risk factor for cardiovascular diseases, and cellular senescence plays a crucial role in this process. Senescence, characterized by irreversible cell cycle arrest and the manifestation of a senescence-associated secretory phenotype (SASP), contributes to the onset and progression of various cardiovascular diseases. Preclinical studies have shown that senolytic drugs effectively remove senescent cells in cardiac and vascular systems, offering potential therapeutic avenues for alleviating cardiovascular diseases. However, more preclinical investigations and clinical trials are needed to assess the safety and efficacy of senolytic treatments. The review highlights the detrimental impact of senescence on various cardiovascular diseases, including systemic atherosclerosis, hypertension, congestive heart failure, arrhythmias, and valvular heart diseases. It also discusses the beneficial effects of senolytics in reducing the burden of senescent cells and improving tissue function. Despite encouraging findings, several questions remain, such as the specific cell types targeted by senolytics and the precise mechanisms through which senescence hinders recovery after myocardial infarction and ischemia-reperfusion injury. Further research is essential to clarify these issues and advance the development of senolytic therapies for cardiovascular diseases.