Targeting AMPK as a potential treatment for hepatic fibrosis in MASLD

Xavier Palomer1, Jue-Rui Wang1, Claudia Escalona1

  • 1Department of Pharmacology, Toxicology, and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, University of Barcelona, 08028 Barcelona, Spain; Institute of Biomedicine of the University of Barcelona (IBUB), University of Barcelona, 08028 Barcelona, Spain; Spanish Biomedical Research Center in Diabetes and Associated Metabolic Diseases (CIBERDEM), Instituto de Salud Carlos III, 28029 Madrid, Spain; Pediatric Research Institute, Hospital Sant Joan de Déu, 08950 Esplugues de Llobregat, Barcelona, Spain.

Insights

AMP-activated protein kinase (AMPK) activation shows promise for treating metabolic dysfunction-associated steatotic liver disease (MASLD) fibrosis. This review explores AMPK

Area of Science:

  • Hepatology and Metabolic Research
  • Molecular Biology
  • Pharmacology

Background:

  • Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent condition often leading to liver fibrosis and failure.
  • Current pharmacological treatments for MASLD-related fibrosis are limited.
  • AMP-activated protein kinase (AMPK) is increasingly recognized as a crucial regulator in fibrogenesis.

Purpose of the Study:

  • To review the molecular mechanisms connecting AMPK to hepatic fibrosis.
  • To evaluate emerging AMPK-directed therapies for MASLD fibrosis.
  • To provide a comprehensive perspective on targeting AMPK for fibrosis treatment.

Main Methods:

  • Literature review of recent mechanistic discoveries and therapeutic developments.
  • Analysis of the role of AMPK in fibrotic pathways.
  • Discussion of clinical translation challenges for AMPK-based therapies.

Main Results:

  • AMPK activation demonstrates potential in mitigating liver fibrosis.
  • Advances in AMPK activators offer new therapeutic avenues.
  • Understanding AMPK's role in fibrogenesis is key to developing effective treatments.

Conclusions:

  • AMPK represents a promising therapeutic target for MASLD-related fibrosis.
  • Further research into AMPK activators and their clinical application is warranted.
  • Targeting AMPK pathways could offer a novel strategy to combat liver fibrosis progression.

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