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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
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.
Abstract:
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease, and often progresses to hepatic fibrosis, cirrhosis, and liver failure. Despite its increasing prevalence, effective pharmacological treatments for MASLD-related fibrosis remain limited. Recent research has highlighted AMP-activated protein kinase (AMPK) as a key regulator of the processes that promote fibrogenesis, and AMPK activation shows potential in mitigating fibrosis. Advances in AMPK activators and deeper insights into their role in fibrotic pathways have recently revitalized interest in targeting AMPK for fibrosis treatment. This review discusses the molecular mechanisms linking AMPK to hepatic fibrosis and evaluates emerging AMPK-directed therapies. Furthermore, it addresses challenges in clinical translation. Importantly, we combine the latest mechanistic discoveries with recent therapeutic developments to provide a comprehensive perspective on AMPK as a target for hepatic fibrosis treatment.
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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