Cellular Senescence Linked to Cardiovascular Aging, Mechanisms and Therapeutic Strategies Under Review
Research indicates that cellular senescence, a state where cells stop dividing but remain metabolically active and secrete inflammatory factors, plays a significant role in cardiovascular aging. This process contributes to endothelial dysfunction, arterial stiffness, myocardial remodeling, and reduced cardiac reserve, increasing susceptibility to conditions like atherosclerosis, hypertension, and heart failure. The review highlights that senescence is not a uniform process; its phenotypes vary based on cell identity, initiating stress, and duration. Key molecular drivers include DNA damage, mitochondrial dysfunction, chronic inflammation, and epigenetic changes. While senescent cells can be cleared by the immune system, prolonged signaling can impair this surveillance. Therapeutic strategies, including senolytics (drugs that remove senescent cells) and senomorphics (drugs that suppress harmful outputs), are being investigated. However, evidence for clinical efficacy in cardiovascular disease is currently l...
