Full text is available at the source.
HIF-1α/BNIP3-Mediated Endoplasmic Reticulum Degradation via Autophagy Protects Against Ischemia Reperfusion-Induced Acute Kidney Injury
Cell Stress Response Protects Kidneys from Damage After Blood Flow Loss and Return
AI simplified
Abstract
HIF-1α and BNIP3 levels increased, activating autophagy and ER degradation in a mouse model of acute kidney injury.
- Knockout of HIF-1α led to decreased BNIP3, autophagy, and ER degradation, worsening kidney injury.
- Overexpression of HIF-1α resulted in increased BNIP3, autophagy, and ER degradation.
- Inhibition of BNIP3 reversed the protective effects of HIF-1α on kidney cells.
- Chloroquine, an autophagy inhibitor, negated the effects of HIF-1α on cell apoptosis.
- Selective overexpression of BNIP3 on the ER membrane enhanced ER degradation through autophagy and reduced cell apoptosis.
AI simplified