Burned mice showed kidney dysfunction, tubular structural damage, and increased tubular cell death, confirming the model was successful. Kidney proteomics revealed a clear separation of protein profiles between the burn group and sham group, with most differential proteins being upregulated. Functional enrichment focused on acute phase response, iron ion transport, ferroptosis, and porphyrin metabolism; ferroptosis-related proteins like ACSL4, FTH1, FTL1, and MT1/2 were upregulated and correlated with KIM1. Western blot and immunohistochemistry confirmed increased expression in the tubular regions. In burned kidneys, lipid peroxidation, MDA, and Fe²⁺ levels were elevated, with electron microscopy showing ferroptosis-like changes such as mitochondrial shrinkage, increased membrane density, and reduced cristae; Fer-1 reversed lipid peroxidation and iron accumulation, reduced tubular cell death, improved tissue pathology and kidney function, and increased survival. In vitro, burn serum induced lipid peroxidation and death in renal tubular epithelial cells, which Fer-1 directly rescued. GPX4 did not decrease concurrently, supporting a non-classical ferroptosis driven by iron overload/ACSL4.

Original link:

doi.org/10.1038/s41419-026-09241-8

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