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Decrease in UCP1 by sustained high lipid promotes NK cell necroptosis to exacerbate nonalcoholic liver fibrosis.

Min Gu1,2, Yu Zhang1,3, Zhijie Lin1,2

  • 1Department of Gastroenterology, Affiliated Hospital of Yangzhou University, Yangzhou, PR China.

Cell Death & Disease
|July 20, 2024
PubMed
Summary

Uncoupling protein 1 (UCP1) deficiency in natural killer (NK) cells impairs their function, worsening nonalcoholic steatohepatitis (NASH) and liver fibrosis. High lipids further reduce UCP1, promoting NK cell death and disease progression.

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Area of Science:

  • Mitochondrial biology
  • Immunology
  • Hepatology

Background:

  • Uncoupling protein 1 (UCP1) is crucial for thermogenesis via mitochondrial proton leak.
  • Compromised natural killer (NK) cell activity is linked to nonalcoholic liver fibrosis.
  • Decreased UCP1 expression in NK cells is observed in advanced nonalcoholic fatty liver disease (NAFLD).

Purpose of the Study:

  • To investigate the role of UCP1 in NK cell function and its contribution to nonalcoholic steatohepatitis (NASH) progression.
  • To elucidate the mechanisms by which UCP1 deficiency and high lipid exposure affect NK cell viability and liver fibrosis.

Main Methods:

  • Utilized UCP1 knockout (UCP1-/-) and floxed mice (UCP1flox/flox-NCR1cre) fed a methionine-choline-diet (MCD).
  • Performed NK cell activity assays, RNA sequencing (RNA-seq), and electron microscopy.
  • Investigated NK cell necroptosis pathways and UCP1 regulation by fatty acids (PA) via the PPARγ/ATF2 axis.

Main Results:

  • UCP1 deficiency in NK cells exacerbated liver fibrosis in MCD-fed mice.
  • UCP1-/- NK cells exhibited impaired bioactivity and enhanced mitophagy-associated gene transcription.
  • Combined UCP1 deficiency and high lipid exposure induced NK cell necroptosis via DRP1S616, with reduced mitophagy.
  • Sustained high palmitic acid (PA) treatment downregulated UCP1 in NK cells via the PPARγ/ATF2 axis.

Conclusions:

  • UCP1 in NK cells plays a protective role against NASH progression to liver fibrosis.
  • Persistent high-lipid exposure decreases UCP1 expression and promotes NK cell necroptosis, contributing to liver fibrosis.
  • Targeting UCP1 in NK cells may offer a therapeutic strategy for NASH-associated liver fibrosis.