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Author Spotlight: Establishing MASLD Cell Models for Investigating Disease Mechanisms and the Lipid-Lowering Effects of Koumiss
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Abnormal ac4C modification in metabolic dysfunction associated steatotic liver cells.

Xiqian Zhang1, Yaxian Zheng1, Jing Yang1

  • 1Department of Pharmacy, Affiliated Hospital of Southwest Jiao Tong University, The Third People's Hospital of Chengdu, Chengdu, 610014, China.

Scientific Reports
|January 6, 2025
PubMed
Summary

N4-acetylcytosine (ac4C) RNA modifications are linked to metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis. This study reveals ac4C changes and identifies key genes, suggesting ac4C as a potential therapeutic target for MASLD.

Keywords:
EpitranscriptomeMASLDac4C

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Metabolic dysfunction-associated steatotic liver disease (MASLD) pathogenesis is complex and not fully understood.
  • The epitranscriptome, including RNA modifications like N4-acetylcytosine (ac4C), is a promising area for understanding disease mechanisms.
  • The role of ac4C in MASLD has not been previously investigated.

Purpose of the Study:

  • To investigate the role and impact of ac4C RNA modifications in the pathogenesis of MASLD.
  • To identify differentially acetylated ac4C sites and differentially expressed genes in a MASLD model.
  • To explore potential therapeutic targets for MASLD based on ac4C modification.

Main Methods:

  • Utilized acRIP-ac4c-seq and RNA-seq in a free fatty acids-induced MASLD cell model.
  • Performed functional enrichment analysis on differentially modified and expressed genes.
  • Constructed a protein-protein interaction (PPI) network using Cytoscape to identify core proteins.

Main Results:

  • Identified 2128 differentially acetylated ac4C sites (1031 hyper, 1097 hypo) in MASLD model cells.
  • Found enrichment of ac4C-modified genes in nuclear transport and MAPK signaling pathways.
  • Discovered 341 differentially expressed genes, enriched in fatty acid biosynthesis, with 118 showing both altered ac4C and expression. Key proteins identified include JUN, CAV1, FASN, and hnRNPA1.

Conclusions:

  • ac4C modification is positively correlated with MASLD pathogenesis.
  • Genes involved in MASLD pathogenesis are significantly affected by ac4C modifications.
  • ac4C modification represents a potential novel therapeutic strategy for MASLD.