INHBA knockdown inhibits renal fibrosis in mice following ischemia-reperfusion injury by suppressing activation of the TGF-β/Smad signaling pathway.

ABSTRACT:

Background

Acute kidney injury (AKI) and renal fibrosis are clinical conditions associated with high morbidity and mortality. Renal ischemia-reperfusion (I/R) injury is a major cause of AKI.

Objective

This study aimed to investigate the role of inhibin subunit beta A (INHBA) in the pathogenesis of renal fibrosis and the underlying mechanisms during I/R-induced kidney injury using an in vivo model.

Methods

A mouse model of renal I/R injury was established. INHBA function was evaluated by intrarenal injection of INHBA-short hairpin RNA (INHBA-shRNA) on day 7 after I/R. Renal function, tubular damage, and interstitial fibrosis were assessed using detection kits, hematoxylin-eosin staining, and Masson's trichrome staining. reverse transcription-quantitative polymerase cha

SUBMITTER: Wang Y 

PROVIDER: S-EPMC12465377 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature