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CRIF1 deficiency induced mitophagy via p66shc-regulated ROS in endothelial cells

Shuyu Piao1, Harsha Nagar1, Seonhee Kim1

  • 1Department of Physiology & Medical Science, College of Medicine, Chungnam National University, Daejeon, 301-747, Republic of Korea.

Biochemical and Biophysical Research Communications
|December 7, 2019
PubMed

Insights

CRIF1 deficiency impairs endothelial cell mitochondrial function, increasing ROS and promoting mitophagy. This process is mediated by the redox enzyme p66shc, highlighting a novel pathway for mitophagy induction.

Area of Science:

  • Cell Biology
  • Mitochondrial Biology
  • Endothelial Cell Function

Background:

  • Mitochondrial dysfunction and oxidative stress are key factors in mitophagy initiation.
  • CR6 interacting factor 1 (CRIF1) plays a role in maintaining mitochondrial function in endothelial cells.

Purpose of the Study:

  • To investigate the mechanism by which CRIF1 deficiency induces mitophagy in human umbilical vein endothelial cells (HUVECs).
  • To explore the role of reactive oxygen species (ROS) and the p66shc enzyme in this process.

Main Methods:

  • Downregulation of CRIF1 in HUVECs.
  • Assessment of mitophagy markers (LC3, PINK1, parkin).
  • Measurement of mitochondrial ROS and membrane potential.
  • Knockdown of p66shc and evaluation of its effects.

Main Results:

  • CRIF1 downregulation increased mitophagy markers and p66shc expression.
  • Mitochondrial ROS scavenging reduced p66shc levels.
  • p66shc knockdown mitigated CRIF1 deficiency-induced mitochondrial dysfunction and mitophagy.

Conclusions:

  • CRIF1 deficiency triggers mitophagy in endothelial cells through a mechanism involving p66shc-regulated ROS.
  • Targeting the CRIF1-p66shc-ROS pathway may offer therapeutic strategies for endothelial dysfunction.
Keywords:
CRIF1MitophagyROSp66shc

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