CYBB-Mediated Ferroptosis Drives Podocyte Injury in Lupus Nephritis and Represents a Therapeutic Target - PubMed
5 hours ago
- #podocyte injury
- #lupus nephritis
- #ferroptosis
- CYBB-mediated ferroptosis is identified as a key driver of podocyte injury in lupus nephritis (LN).
- Ferroptosis markers (iron overload, lipid peroxidation, glutathione depletion, GPX4 downregulation) were observed in MRL/lpr mice, leading to podocyte loss and proteinuria.
- Ferrostatin-1 (Fer-1) treatment significantly improved renal pathology and preserved podocyte integrity.
- Bioinformatic analysis identified CYBB as a ferroptosis-related hub gene upregulated in LN, correlating with renal dysfunction and oxidative injury.
- CYBB overexpression enhanced ROS generation and ferroptotic podocyte damage, while CYBB knockdown or Fer-1 reversed these effects.
- Both pharmacological and genetic inhibition of CYBB mitigated ferroptosis, preserved podocyte integrity, and improved renal function, highlighting CYBB as a promising therapeutic target in LN.