Ferroptosis activation contributes to kidney aging in mice by promoting tubular cell senescence.

Kidney aging is the strongest independent risk factor for chronic kidney disease. Ferroptosis, a recently discovered form of cell death mediated by iron overload and lipid peroxidation accumulation, has an unclear role in kidney aging. To determine the pathophysiological role of ferroptosis during kidney aging, we employed immunofluorescence, western blotting, and qRT‒PCR to analyze renal cells and tissues in natural aging and accelerated aging mouse models.

Inhibition of ACSL4 ameliorates tubular ferroptotic cell death and protects against fibrotic kidney disease.

Ferroptosis is a recently recognized form of regulated cell death, characterized by iron-dependent accumulation of lipid peroxidation. Ample evidence has depicted that ferroptosis plays an essential role in the cause or consequence of human diseases, including cancer, neurodegenerative disease and acute kidney injury. However, the exact role and underlying mechanism of ferroptosis in fibrotic kidney remain unknown.