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This article is career advice for PhD students and has no relevance to longevity, health, or medical research.
Biological age reversal, epigenetic clocks, senolytics, and anti-aging interventions
1.644 artigos
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.
A new review links interoception — the body's ability to sense internal states — directly to aging mechanisms and homeostatic decline.
A 2-year study of 100 healthy adults reveals four distinct, stable immunotypes shaped by innate immune activity—not just age, sex, or CMV status.