Cardiovascular diseases (CVDs) are the leading cause of death worldwide, with a significant impact on patient quality of life and disability. The increasing prevalence of age-related CVDs, such as atherosclerosis, coronary artery stenosis, myocardial infarction (MI), valvular heart disease, and heart failure (HF), will contribute to a greater health and economic burden as global life expectancy increases. Cellular senescence and mitochondrial dysfunction are key mechanisms underlying CVD. Cellular senescence, initially defined as irreversible exit from the cell cycle, now includes characteristics such as mitochondrial dysfunction, resistance to apoptosis, and the activation of the senescence-associated secretory phenotype (SASP). Mitochondrial dysfunction, characterized by energy starvation, oxidative stress, mitochondrial dynamics imbalance, and increased ROS production, is crucial in CVD. Therapeutic approaches targeting mitochondrial dysfunction, such as AMPK activation with metformin and ROS reduction with antioxidants like CoQ10, have shown promise. Senolytics, which target anti-apoptotic pathways to eliminate senescent cells, and senomorphics, which modulate the senescent phenotype, are also being explored. Understanding the interconnected phenomena of mitochondrial dysfunction, oxidative stress, and senescence will enable the development of novel therapies for CVD.Cardiovascular diseases (CVDs) are the leading cause of death worldwide, with a significant impact on patient quality of life and disability. The increasing prevalence of age-related CVDs, such as atherosclerosis, coronary artery stenosis, myocardial infarction (MI), valvular heart disease, and heart failure (HF), will contribute to a greater health and economic burden as global life expectancy increases. Cellular senescence and mitochondrial dysfunction are key mechanisms underlying CVD. Cellular senescence, initially defined as irreversible exit from the cell cycle, now includes characteristics such as mitochondrial dysfunction, resistance to apoptosis, and the activation of the senescence-associated secretory phenotype (SASP). Mitochondrial dysfunction, characterized by energy starvation, oxidative stress, mitochondrial dynamics imbalance, and increased ROS production, is crucial in CVD. Therapeutic approaches targeting mitochondrial dysfunction, such as AMPK activation with metformin and ROS reduction with antioxidants like CoQ10, have shown promise. Senolytics, which target anti-apoptotic pathways to eliminate senescent cells, and senomorphics, which modulate the senescent phenotype, are also being explored. Understanding the interconnected phenomena of mitochondrial dysfunction, oxidative stress, and senescence will enable the development of novel therapies for CVD.