Biological age reversal, epigenetic clocks, senolytics, and anti-aging interventions
1245 articles
A landmark review reveals why aging immune systems lose the ability to clear senescent cells — and how new therapies could restore this critical defense.
A landmark NIH-funded consortium is building the first reference atlas of somatic mutations across healthy human tissues to decode aging and disease.
New research shows taurine suppresses p53-driven senescence in pancreatic β-cells, offering a potential strategy to preserve insulin secretion with age.
A novel SQSTM1-mediated selective autophagy pathway degrades p16 and p21, reducing cellular senescence in degenerative mitral valve disease.
A 2025 review reveals how two sulfur-based amino acids act as master regulators of cellular redox balance and age-related decline.
A new study shows ferroptosis drives cellular senescence, and blocking it with ferrostatin-1 extends lifespan and healthspan in worms and aging mice.
GH drops sharply as we age, mimicking deficiency states — yet boosting it in older adults shows mixed results and real risks.
A longitudinal study of 54 adults finds COVID-19 infection significantly accelerates biological aging across multiple epigenetic clocks.
A new mouse study shows fisetin senolytic treatment reverses age-related endothelial dysfunction by eliminating senescent cells and reducing the SASP factor CXCL12.
Fisetin encapsulated in liposomes significantly reduces IL-6 and IL-8 secretion in senescent lung cells, revealing potent senomorphic but not senolytic activity.
A new review finds kaempferol, a common dietary flavonoid, acts as a senolytic agent and produces dose-dependent hormetic effects tied to aging biology.
A 2025 comprehensive review maps how the AMPK/SIRT1/PGC-1α axis controls energy balance and drives neurodegeneration, diabetes, and cardiovascular disease.
