Cardiac cell senescence is a natural process that occurs with aging, leading to a decline in heart function and contributing to heart failure. This review summarizes the molecular mechanisms, key proteins, and therapeutic targets involved in cardiac cell senescence. It discusses the molecular modulators of cellular senescence in aging hearts and explores potential drug targets for intervention. The review highlights the role of various cell types, including cardiomyocytes, endothelial cells, fibroblasts, and vascular smooth muscle cells, in the senescence process. Senescence in these cells leads to structural and functional changes in the heart, contributing to age-related cardiovascular diseases. The review also discusses the molecular pathways involved in cardiac senescence, such as telomere shortening, oxidative stress, and metabolic dysregulation. Key proteins and signaling pathways, including p53, p16, and SIRT1, are highlighted as important regulators of cardiac senescence. The review also explores the role of epigenetic modifications, such as DNA methylation and histone modifications, in cardiac senescence. Potential therapeutic strategies targeting these pathways are discussed, including the use of sirtuins, AMPK, and other metabolic regulators. The review emphasizes the importance of understanding the molecular mechanisms of cardiac senescence to develop effective interventions for age-related cardiovascular diseases.Cardiac cell senescence is a natural process that occurs with aging, leading to a decline in heart function and contributing to heart failure. This review summarizes the molecular mechanisms, key proteins, and therapeutic targets involved in cardiac cell senescence. It discusses the molecular modulators of cellular senescence in aging hearts and explores potential drug targets for intervention. The review highlights the role of various cell types, including cardiomyocytes, endothelial cells, fibroblasts, and vascular smooth muscle cells, in the senescence process. Senescence in these cells leads to structural and functional changes in the heart, contributing to age-related cardiovascular diseases. The review also discusses the molecular pathways involved in cardiac senescence, such as telomere shortening, oxidative stress, and metabolic dysregulation. Key proteins and signaling pathways, including p53, p16, and SIRT1, are highlighted as important regulators of cardiac senescence. The review also explores the role of epigenetic modifications, such as DNA methylation and histone modifications, in cardiac senescence. Potential therapeutic strategies targeting these pathways are discussed, including the use of sirtuins, AMPK, and other metabolic regulators. The review emphasizes the importance of understanding the molecular mechanisms of cardiac senescence to develop effective interventions for age-related cardiovascular diseases.