It seems perhaps overly reductionist to summarize the panoply of current efforts to treat aging into two camps of (a) things that affect the burden of cellular senescence and (b) things that affect metabolism. One has to cut out or diminish the importance of a fair number of line items that may be useful irrespective of their effects on cellular senescence. An increased burden of cellular senescence is only one of the major issues that drive aging. Nonetheless, that is the approach to categorization taken in this review paper.
Aging is a complex biological process characterized by progressive functional decline, driving the incidence of age-related diseases such as neurodegeneration, metabolic disorders, and cardiovascular diseases. Therapeutic strategies targeting aging hallmarks can delay aging and mitigate disease risk. Emerging interventions focus on modulating core aging mechanisms, including cellular senescence, metabolic dysfunction, epigenetic alterations, and mitochondrial impairment, etc.
Recent advances have focused on three strategies: senolytics (eliminating senescent cells, e.g., dasatinib + quercetin), senomorphics (inhibiting the senescence-associated secretory phenotype, e.g., rapamycin), and senoreversion (rejuvenating senescent cells via epigenetic reprogramming). Additionally, metabolic interventions such as caloric restriction mimetics (e.g., spermidine, α-ketoglutarate, ergothioneine) enhance mitochondrial function, activate autophagy, and reprogram energy metabolism, demonstrating lifespan extension and healthspan improvement in preclinical models. Collectively, these approaches hold promise for delaying aging and alleviating age-related pathologies, facilitating the transition to precision longevity medicine.
Link: https://doi.org/10.1038/s41392-026-02662-z
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