Anti-aging processes

Anti-aging processes comprise a complex network of biological mechanisms intended to maintain cellular homeostasis and mitigate the physiological decline associated with chronological age. These processes are centered on the 'Hallmarks of Aging,' which include genomic instability, telomere attrition, epigenetic alterations, and loss of proteostasis (López-Otín et al., 2013/2023, Cell). At the molecular level, these processes involve nutrient-sensing pathways such as the mechanistic target of rapamycin (mTOR), adenosine monophosphate-activated protein kinase (AMPK), and sirtuins, which coordinate cellular responses to energy availability and environmental stress (National Institute on Aging). In disease contexts, the failure of these endogenous anti-aging systems leads to the accumulation of cellular damage and senescent cells, driving chronic conditions like neurodegeneration and cardiovascular disease. Pharmacological interventions targeting these processes, known as geroprotectors, aim to delay or reverse age-related pathologies by mimicking calorie restriction or enhancing cellular repair (PubMed, PMC6562082). For example, drugs like metformin and rapamycin modulate metabolic signaling to improve healthspan, while senolytics like dasatinib and quercetin selectively eliminate damaged cells that secrete pro-inflammatory factors (StatPearls). While promising, therapeutic modulation of anti-aging processes faces challenges regarding systemic side effects, such as potential immunosuppression or interference with normal tissue regeneration. Consequently, 'Anti-aging processes' is not a single therapeutic target but rather a broad category of biological pathways requiring specific molecular characterization for drug development.

Other names

Longevity pathwaysGeroprotective mechanismsHallmarks of agingCellular rejuvenationBiological mechanisms of aging

Modulation of evolutionary conserved nutrient-sensing pathways (mTOR inhibition, AMPK activation, Sirtuin activation), removal of senescent cells (senolysis), enhancement of mitochondrial biogenesis, and restoration of proteostatic mechanisms.