Geriatrics (Basel, Switzerland) · 2026
Aging as Loss of Biological Self-Correction: A Geroscience Framework for Longevity, Inflammaging, and Restored Resilience.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Bar-Or David, Williams Jason, Paredes Daniel
Аннотация
Longevity science has shifted from the pursuit of lifespan extension toward preservation of healthspan, resilience, and functional independence. The hallmarks of aging provide a powerful descriptive structure, but they do not by themselves specify how diverse molecular defects translate into loss of adaptive function. We propose a complementary conceptual framework in which aging is viewed as progressive impairment of biological self-correction: the distributed capacity to sense consequential perturbations, scale an appropriate response, repair or remove damage, terminate the response, and recover or adaptively re-equilibrate while preserving future functional reserve. This framework is not intended to replace homeostasis, homeodynamics, allostasis, physiological reserve, or resilience; rather, it links these established concepts to the molecular machinery that generates dynamic recovery. Correction fidelity is proposed to be measured independently of the hallmarks using stress-response trajectories, including response latency, magnitude of deviation, recovery slope or half-time, integrated deviation, residual deficit, overshoot, biological cost, final functional state, and preservation of subsequent reserve. Importantly, successful recovery need not mean return to a fixed youthful baseline because aging may also shift the physiological setpoint toward a less favorable but actively defended equilibrium. We integrate evolutionary and biodemographic principles with inflammaging, nutrient sensing, NAD+ biology, senescence, autophagy, partial reprogramming, and resilience research, and propose falsifiable predictions for testing whether dynamic recovery adds information beyond chronological age, frailty, and static aging biomarkers.