Cellular senescence and mitochondrial dysfunction are key contributors to cardiovascular disease (CVD). Senescence, initially defined as irreversible cell cycle exit, now includes mitochondrial dysfunction, resistance to apoptosis, and the senescence-associated secretory phenotype (SASP). Senescent cells, such as cardiomyocytes, can become senescent and contribute to CVD pathophysiology, including myocardial remodelling, hypertension, atherosclerosis, and aortic aneurysms. Mitochondrial dysfunction in CVD leads to reduced ATP production, increased reactive oxygen species (ROS), and mitochondrial dynamic imbalance. Energy starvation and oxidative stress are major consequences of mitochondrial dysfunction, with ROS playing a critical role in inducing senescence and contributing to telomere attrition and DNA damage. Mitochondrial dysfunction is also linked to increased ROS production, which can drive further mitochondrial damage and senescence, creating a cyclical interaction between mitochondrial dysfunction, oxidative stress, and senescence. Mitochondrial dynamics, including fusion and fission, are essential for maintaining mitochondrial function and quantity. Disruptions in these processes are associated with CVD. Mitophagy, the selective degradation of damaged mitochondria, is crucial for maintaining mitochondrial health and preventing the accumulation of dysfunctional mitochondria. Impaired mitophagy is linked to CVD and increased oxidative stress. Senescent cells also express pro-survival pathways that enhance resistance to apoptosis, contributing to their persistence and the secretion of SASP factors, which promote inflammation and tissue dysfunction. Therapeutic strategies targeting mitochondrial dysfunction and senescence include drugs like metformin, which improves mitochondrial function and reduces oxidative stress, and mitochondrial-targeted antioxidants like MitoQ, which reduce ROS and improve cardiac function. Senolytics, such as dasatinib and quercetin, and senomorphics, which modulate SASP, are emerging therapies that may help eliminate or reduce the impact of senescent cells in CVD. These approaches highlight the importance of targeting mitochondrial dysfunction and senescence to improve cardiovascular health and prevent age-related diseases.Cellular senescence and mitochondrial dysfunction are key contributors to cardiovascular disease (CVD). Senescence, initially defined as irreversible cell cycle exit, now includes mitochondrial dysfunction, resistance to apoptosis, and the senescence-associated secretory phenotype (SASP). Senescent cells, such as cardiomyocytes, can become senescent and contribute to CVD pathophysiology, including myocardial remodelling, hypertension, atherosclerosis, and aortic aneurysms. Mitochondrial dysfunction in CVD leads to reduced ATP production, increased reactive oxygen species (ROS), and mitochondrial dynamic imbalance. Energy starvation and oxidative stress are major consequences of mitochondrial dysfunction, with ROS playing a critical role in inducing senescence and contributing to telomere attrition and DNA damage. Mitochondrial dysfunction is also linked to increased ROS production, which can drive further mitochondrial damage and senescence, creating a cyclical interaction between mitochondrial dysfunction, oxidative stress, and senescence. Mitochondrial dynamics, including fusion and fission, are essential for maintaining mitochondrial function and quantity. Disruptions in these processes are associated with CVD. Mitophagy, the selective degradation of damaged mitochondria, is crucial for maintaining mitochondrial health and preventing the accumulation of dysfunctional mitochondria. Impaired mitophagy is linked to CVD and increased oxidative stress. Senescent cells also express pro-survival pathways that enhance resistance to apoptosis, contributing to their persistence and the secretion of SASP factors, which promote inflammation and tissue dysfunction. Therapeutic strategies targeting mitochondrial dysfunction and senescence include drugs like metformin, which improves mitochondrial function and reduces oxidative stress, and mitochondrial-targeted antioxidants like MitoQ, which reduce ROS and improve cardiac function. Senolytics, such as dasatinib and quercetin, and senomorphics, which modulate SASP, are emerging therapies that may help eliminate or reduce the impact of senescent cells in CVD. These approaches highlight the importance of targeting mitochondrial dysfunction and senescence to improve cardiovascular health and prevent age-related diseases.