Aging-driven deterioration in cellular repair, molecular damage clearance, and resilience mechanisms accelerates atherosclerosis and cardiovascular disease (CVD) — the world's leading cause of death. This review from Athens synthesizes how geroscience — the discipline bridging aging biology and clinical medicine — frames CVD not as an isolated organ failure but as a downstream consequence of systemic aging. Key targets discussed include multimorbidity, sarcopenia, frailty, cardiac arrhythmias, cognitive decline, undernutrition, and polypharmacy, with emphasis on both pharmacological (gerotherapeutics) and nonpharmacological interventions, particularly exercise and dietary pattern modification.
The framing here matters more than the individual findings. Geroscience's core proposition — that treating aging itself is more efficient than chasing individual diseases — is gaining traction in cardiology and geriatrics, yet remains underimplemented clinically. The practical implication for adults is meaningful: physical activity remains the most evidence-dense, lowest-risk intervention addressing nearly every mechanism discussed, from mitochondrial efficiency to inflammatory load to sarcopenia reversal. The review's breadth is also its limitation — as a narrative synthesis rather than original data, it cannot quantify effect sizes or establish causality. Its value lies in consolidating the geroscience paradigm for clinical audiences. Incremental rather than paradigm-shifting as a standalone contribution, but reflects a genuinely important conceptual shift in how cardiovascular aging should be managed preventively across the lifespan.
