PPARγ agonism ameliorates acute kidney injury by inhibiting neutrophil extracellular trap formation-mediated renal tubular epithelial cell PANoptosis.

ABSTRACT:

Background

Cisplatin (CP)-induced nephrotoxicity is a major clinical concern. Emerging evidence has revealed the critical role of PANoptosis, a coordinated cell death pathway, and neutrophil extracellular traps (NETs) in renal tubular damage. The nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) has been recognized as a potential modulator of inflammation and cell survival; however, its regulatory function and mechanism in acute kidney injury (AKI), especially CP-induced AKI, particularly concerning NETs and PANoptosis, remain poorly understood. This study investigates the central role of PPARγ and explores the therapeutic potential of its novel activator, O-alkyl and o-benzyl hesperetin derivative-1 L (HD-1L), in this context.

Methods

Cultured renal

SUBMITTER: Du C 

PROVIDER: S-EPMC12910742 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature