Cardiac cell senescence is a critical process in cardiac aging, leading to reduced heart function and increased risk of heart failure. This review explores the molecular mechanisms, key proteins, and therapeutic targets involved in cardiac cell senescence. It discusses the role of various cellular and molecular factors, including telomere shortening, oxidative stress, and inflammatory signaling, in the senescence of cardiomyocytes, endothelial cells, fibroblasts, and vascular smooth muscle cells. The review highlights the importance of cellular senescence in the development of age-related cardiovascular diseases and the potential for targeting these processes to improve cardiac function. Key proteins and pathways, such as p53, p16, and SIRTs, are discussed as potential therapeutic targets. The review also emphasizes the role of the local microenvironment in modulating cardiac senescence and the impact of metabolic changes, epigenetic modifications, and circadian rhythms on the aging heart. Overall, the review provides a comprehensive understanding of the molecular mechanisms underlying cardiac senescence and offers insights into potential therapeutic strategies for mitigating age-related cardiac dysfunction.Cardiac cell senescence is a critical process in cardiac aging, leading to reduced heart function and increased risk of heart failure. This review explores the molecular mechanisms, key proteins, and therapeutic targets involved in cardiac cell senescence. It discusses the role of various cellular and molecular factors, including telomere shortening, oxidative stress, and inflammatory signaling, in the senescence of cardiomyocytes, endothelial cells, fibroblasts, and vascular smooth muscle cells. The review highlights the importance of cellular senescence in the development of age-related cardiovascular diseases and the potential for targeting these processes to improve cardiac function. Key proteins and pathways, such as p53, p16, and SIRTs, are discussed as potential therapeutic targets. The review also emphasizes the role of the local microenvironment in modulating cardiac senescence and the impact of metabolic changes, epigenetic modifications, and circadian rhythms on the aging heart. Overall, the review provides a comprehensive understanding of the molecular mechanisms underlying cardiac senescence and offers insights into potential therapeutic strategies for mitigating age-related cardiac dysfunction.