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Although acute senescence contributes beneficially to tumor suppression and wound healing, chronic accumulation of senescent cells sustains systemic inflammaging and accelerates organ dysfunction. This review synthesizes current progress in aging biology into a unified mechanistic and translational framework. We first examine how primary aging hallmarks, such as genomic instability and epigenetic dysregulation, interact to trigger cellular senescence, then explore how these converging molecular processes give rise to distinct age\u2010related pathologies across reproductive, pulmonary, hepatic, neurological, skeletal, and metabolic systems. We further evaluate emerging interventional strategies, from senolytics and senomorphics to rejuvenation approaches, while addressing key translational barriers including targeting specificity, senescence heterogeneity, and equitable access. 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