HIF-1α/BNIP3-Mediated Endoplasmic Reticulum Degradation via Autophagy Protects Against Ischemia Reperfusion-Induced Acute Kidney Injury

Aug 5, 2024Antioxidants & redox signaling

Cell Stress Response Protects Kidneys from Damage After Blood Flow Loss and Return

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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.

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