IgA nephropathy is the most common primary glomerulonephritis worldwide. In a mouse study, antroquinonol, a purified compound from Antrodia camphorata mycelium, switched three pathways at once, activating Nrf2, restraining T cells, and silencing the NLRP3 inflammasome, easing kidney damage.
## Why some liver cells survive a chemical hit Loganin, a modest iridoid glycoside from Cornus fruit, helps liver cells endure chemical assault by flipping two
Four 2026 studies converge on one conclusion: brain aging is not the brain's problem alone. Peripheral CD8⁺ EMRA T-cell immunosenescence, plasma glucose with Mendelian Randomization causal evidence, and arterial wall cellular heterogeneity collapse are converging on the aging brain — while intracranial microglia and oligodendrocytes inflammage in near-perfect synchrony (Pearson r≈0.98). Understanding this multi-source siege reframes what prevention might realistically look like.
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.
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.
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.