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Reduction in Hepatic Phosphatidylcholine Biosynthesis Promotes MASH Through Copper Deficiency.

Jaclyn E Welles1,2, James P Garifallou3, Michael V Gonzalez3

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Metabolic dysfunction-associated steatohepatitis (MASH) involves impaired phosphatidylcholine (PC) biosynthesis, leading to copper (Cu) redistribution. This Cu dysregulation promotes liver fibrosis by activating hepatic stellate cells.

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Metabolic Disorders

Background:

  • Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease characterized by lipid dysregulation and fibrosis.
  • The precise mechanisms linking altered lipid metabolism, specifically reduced hepatic phosphatidylcholine (PC), to MASH progression and fibrosis remain unclear.

Purpose of the Study:

  • To investigate the role of copper (Cu) homeostasis in MASH pathogenesis, particularly its connection to impaired PC biosynthesis.
  • To elucidate how Cu redistribution affects hepatic stellate cell activation and liver fibrosis in MASH.

Main Methods:

  • Utilized complementary genetic and dietary mouse models of MASH.
  • Employed single-nucleus RNA sequencing to analyze hepatic gene expression.
  • Investigated the effects of Cu modulation (supplementation and chelation) on MASH parameters in vivo and in vitro.

Main Results:

  • Reduced hepatic PC in MASH models correlated with hepatic Cu depletion and increased circulating Cu, indicating disrupted Cu distribution.
  • PC depletion impaired hepatocyte copper uptake by affecting CTR1 localization, while Cu promoted fibrogenic activation of human hepatic stellate cells.
  • Liver-directed Cu supplementation reduced steatosis but not fibrosis, whereas Cu chelation with bathocuproinedisulfonic acid (BCS) reduced fibrosis.

Conclusions:

  • Impaired PC biosynthesis in MASH leads to Cu redistribution, impacting hepatic stellate cell activation and fibrogenesis.
  • Cu-dependent signaling plays a significant role in MASH pathogenesis, particularly in promoting liver fibrosis.