Biological age reversal, epigenetic clocks, senolytics, and anti-aging interventions
1634 articoli
Scendi in profondità nel pathway PI3K per comprendere come i messaggeri fosfolipidici, le cascate chinasiche e i circuiti di feedback plasmano l'equilibrio tra crescita e longevità.
A study of 1.1 million adults shows frailty deficits accumulate in sudden bursts—and these episodes signal sharply higher risk of death and hospitalization.
This article is career advice for PhD students and has no relevance to longevity, health, or medical research.
A comprehensive review maps the key drug strategies targeting mitochondrial dysfunction in aging and neurodegenerative diseases.
A mitochondria-targeting peptide restores cardiac and skeletal muscle function in aging mice—but leaves epigenetic and transcriptomic age unchanged.
P16+ senescent fibroblasts and macrophages hijack immune signaling post-infarction, driving deadly cardiac remodeling through a newly identified CCL8 pathway.
A crystal structure reveals DLK1 mimics TGF-β ligands to block myostatin signaling, reshaping our understanding of muscle development.
Semaglutide loses ~45% lean mass per kg lost vs. 25% for tirzepatide. Experts weigh interventions to protect muscle in aging patients.
Mendelian randomization reveals longer telomeres reduce Alzheimer's risk by 16%, with nine brain structural changes partially explaining the link.
The circadian CLOCK protein plays a dual role in cellular senescence — supporting healthy aging in normal cells while enabling tumor growth when hijacked.
TOP3A topoisomerase is essential for ALT, a telomere-maintenance pathway used by 10–15% of cancers, opening new therapeutic targets.
Short-term rapamycin causes temporary thymic involution, then triggers regeneration exceeding baseline — hinting at immune rejuvenation as a longevity mechanism.
