Fisetin Clears Senescent Cells and Restores Blood Vessel Function via CXCL12
A new mouse study shows fisetin senolytic treatment reverses age-related endothelial dysfunction by eliminating senescent cells and reducing the SASP factor CXCL12.
Biological age reversal, epigenetic clocks, senolytics, and anti-aging interventions
1273 articles
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.
RA patients show accelerated immune aging in T cells, B cells, and myeloid cells—predating joint inflammation and directly fueling autoimmunity.
A completed Phase 2 trial investigates the immune mechanisms behind age-related vaccine failure in older adults.
Chronic NAD depletion causes mitochondrial DNA to escape into the cytoplasm, activating an interferon response that mimics a viral infection.
A specialized immune cell population near adipose nerves declines with age, fueling inflammaging and disrupting fat metabolism.
A comprehensive 2025 review reveals how AMPK orchestrates mitochondrial fission, mitophagy, and biogenesis to restore cellular energy homeostasis.
A lysosome-to-epigenome pathway in C. elegans extends lifespan across multiple generations via histone H3.3 transport from gut to germline.
A 2026 review maps the molecular architecture of telomerase across four model organisms, illuminating cancer and aging disease mechanisms.
Middle-aged marathon runners showed 2.06-fold higher hTERT expression and significant cardiac adaptations compared to inactive controls.