Why do senescent cells persist as organisms grow older? A 2026 Nature Aging study shows that declining chaperone-mediated autophagy (CMA) alters the senescent secretome and blunts macrophage engulfment via SIRPα and CD47 signaling. While pharmacological CMA activation reduced senescent cell burden and fibrosis severity in mice, the findings remain strictly preclinical.
A 2026 study connects mitochondrial protein quality control to oocyte competence during ovarian aging. In mice and a small human oocyte maturation experiment, loss of ClpX increased unfolded proteins and linked to PTGDS/PGD2 signaling, while the experimental inhibitor AT-56 improved several maturation readouts. The findings are mechanistic, not a fertility treatment.
A Nature Cardiovascular Research mouse and cell study finds that aging thins cardiac lymphatics and tightens their junctions, making immune cells and waste harder to clear. Nuclear IL-33 and falling VEGFC are the mechanistic clues. Restoring VEGFC rebuilt vessel density and cut macrophages, but did not fix diastolic function. This is not proof of a human therapy.
A 2025 review places mitochondria at the center of ferroptosis: four firewalls decide whether cancer cells die by lipid peroxidation. This is a mechanism map, not proof of human benefit.
A mouse and cell study links rapamycin with lower atrial fibrillation susceptibility in an accelerated-aging model, pointing to HIF-1α and mitochondrial metabolism. The findings are mechanistic clues, not proof of human benefit or a reason to self-medicate.
113 studies. Clear biological activity, inconclusive clinical benefit. A close read of the 2026 PRISMA review: what NR/NMN actually do, what they don't, and what often gets left out of the conversation.
A blue pill that might protect your brain, and a fiber classification system that's been misleading you for decades. Two stories about how oversimplified categories can steer us wrong.
Recent large-scale genetic analyses shatter the 'longevity gene' myth: the same genetic variant that lowers mortality in youth can increase risk in old age. From antagonistic pleiotropy to circadian rhythms, hippocampal plasticity, and cross-organ aging axes, unpacking the temporal tug-of-war of aging.
Fifty years of antioxidant trials mostly failed because 85% of mitochondrial DNA damage comes from replication errors, not free radicals. From mitochondrial transplantation and MOTS-c peptide hormones to CoQ10's irreplaceable role in the electron transport chain, aging science is moving from 'slow the damage' to 'replace the parts.
The pitch writes itself: as you age, cellular NAD+ levels decline, mitochondria lose their fuel, and muscles begin to waste away. Take NMN or NR daily, restore