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.
Open →Ferroptosis and pyroptosis are two forms of cell death that rupture and splash pro-inflammatory cargo onto neighboring cells. Four 2026 studies — spanning skin fibroblasts, brain microglia and neurons, and diabetic kidneys — trace the same self-amplifying loop and identify three brake points: HIF-1α, stem-cell-secreted TSG-6, and puerarin's control of caspase-1.
Open →Mitophagy — the cell's recycling system for damaged mitochondria — slows with age, letting broken units pile up and leak bacterial-like mtDNA that triggers chronic inflammation. Four 2026 studies show restarting this pathway in rheumatoid arthritis and Alzheimer's models suppresses downstream inflammasome activation, while a fourth study reveals selective autophagy extends well beyond mitochondria.
Open →Aging cells leak R-loops and other nucleic acids into the cytoplasm, tripping cGAS-STING and NLRP3 alarms that keep inflammation burning. Three 2026 studies point to the switches and brakes behind inflammaging.
Open →Senescent cells pile up because aging immune systems stop clearing them efficiently. Instead of killing every senescent cell, new 2026 reviews argue for senomorphic strategies that quiet SASP-driven inflammation.
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