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Related Experiment Video

Updated: May 7, 2025

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Liver B Cells Promotes MASLD Progression via the Apelin/APLNR System.

Su Jiang1, Jiaxue Lu1, Nan Li1

  • 1Department of Medical Laboratory Science, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China.

International Journal of Medical Sciences
|January 2, 2025
PubMed
Summary

The apelin/APLNR axis is upregulated in metabolic dysfunction-associated steatotic liver disease (MASLD), driving disease progression. Targeting this pathway may offer new therapies for MASLD by modulating liver B cell function.

Keywords:
B cellsapelin/APLNRmetabolic dysfunction-associated steatotic liver disease

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Area of Science:

  • Hepatology
  • Metabolic Disorders
  • Immunology

Background:

  • Metabolic dysfunction-associated steatotic liver disease (MASLD) encompasses a spectrum from simple steatosis (MASS) to steatohepatitis (MASH) and fibrosis.
  • The apelin/APLNR axis, a peptide-receptor system, has emerging roles in metabolic regulation and liver disease.
  • The specific involvement of the apelin/APLNR axis and liver B cells in MASLD progression remains incompletely understood.

Purpose of the Study:

  • To investigate the role of the apelin/APLNR axis in MASLD pathogenesis.
  • To examine the axis's impact on the transition from MASS to MASH and fibrosis.
  • To elucidate the influence of the apelin/APLNR axis on liver B cell function in MASLD.

Main Methods:

  • Analysis of serum apelin and APLNR protein levels in MASLD patients.
  • Assessment of liver tissue from hepatocellular carcinoma patients.
  • Development and analysis of C57BL/6J mouse models mimicking various MASLD stages.
  • RNA sequencing of the Raji B cell line to study apelin/APLNR axis regulation.

Main Results:

  • Apelin and APLNR expression are elevated in MASLD patients and correlate with disease severity.
  • Modulation of the apelin/APLNR axis in mouse models impacts liver steatosis, inflammation, and fibrosis.
  • In vitro studies show the apelin/APLNR axis promotes inflammatory cytokine and extracellular matrix gene expression in B cells.

Conclusions:

  • The apelin/APLNR axis plays a critical role in the progression of MASLD.
  • Targeting the apelin/APLNR axis presents a potential therapeutic strategy for MASLD.
  • Modulating B cell activity via this axis could mitigate MASLD advancement.