CAV1 promotes epithelial-to-mesenchymal transition (EMT) and chronic renal allograft interstitial fibrosis by activating the ferroptosis pathway.

ABSTRACT:

Background

Chronic allograft dysfunction (CAD) stands as a critical factor that limits the long-term viability of transplanted kidneys. Ferroptosis is an iron-dependent form of programmed cell death increasingly linked to chronic fibrosis. However, the mechanism by which ferroptosis contributes to the onset and progression of CAD remains unclear.

Methods

This study analyzed transcriptome data from renal transplant biopsy samples in the Gene Expression Omnibus (GEO), through clinical samples, animal models, and cell experiments, this study investigated the mechanism by which Caveolin-1 (CAV1) promotes CAD through the regulation of the ferroptosis pathway.

Results

The elevated levels of CAV1 were found to positively correlate with CAD incidence. Clinical and animal mode

SUBMITTER: Han Q 

PROVIDER: S-EPMC11860899 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature