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NLRX1/FUNDC1/NIPSNAP1-2 axis regulates mitophagy and alleviates intestinal ischaemia/reperfusion injury

Shaoqin Li1, Yi Zhou1, Xiaocheng Gu1

  • 1Department of Interventional and Vascular Surgery, Changzhou No. 2 People's Hospital, Changzhou, China.

Cell Proliferation
|January 12, 2021
PubMed
Abstract

Insights

NOD-like receptor X1 (NLRX1) protects against intestinal injury by regulating mitophagy. NLRX1 downregulation impairs mitophagy, leading to cell damage, while its overexpression promotes resistance to injury.

Area of Science:

  • Mitochondrial biology
  • Gastroenterology
  • Cellular stress response

Background:

  • Mitophagy is crucial in intestinal ischemic reperfusion (IR) injury pathogenesis.
  • NOD-like receptor X1 (NLRX1), a mitochondrial protein highly expressed in the intestine, influences ROS, mitochondrial damage, autophagy, and apoptosis.
  • The specific role of NLRX1 in intestinal IR injury remains to be elucidated.

Purpose of the Study:

  • To investigate the function of NLRX1 in intestinal IR injury.
  • To elucidate the molecular mechanism by which NLRX1 regulates mitochondrial homeostasis and cell apoptosis in the context of intestinal IR.

Main Methods:

  • Western blotting, real-time PCR, and immunohistochemistry were used to measure NLRX1 levels in rats and IEC-6 cells subjected to IR and hypoxia-reoxygenation (HR) injury, respectively.
  • In vitro studies assessed the role of the NLRX1-FUNDC1-NIPSNAP1/NIPSNAP2 axis in mitochondrial homeostasis and apoptosis.
  • Immunoprecipitation was employed to study protein interactions.

Main Results:

  • NLRX1 expression was significantly downregulated following intestinal IR injury.
  • Overexpression of NLRX1 in rats conferred resistance to intestinal IR injury and mitochondrial dysfunction, dependent on mitophagy activation.
  • HR injury reduced NLRX1, promoting FUNDC1 phosphorylation, which inhibited the interaction with NIPSNAP1/NIPSNAP2, thus blocking mitophagy and causing mitochondrial accumulation and epithelial apoptosis.

Conclusions:

  • NLRX1 plays a protective role in intestinal IR injury by regulating mitophagy through the FUNDC1-NIPSNAP1/NIPSNAP2 signaling pathway.
  • Targeting NLRX1 offers a potential therapeutic strategy for mitigating intestinal IR injury.
Keywords:
FUNDC1NIPSNAP1-2NLRX1hypoxia reoxygenation injuryischaemia reperfusion injurymitophagy

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