•  2025 Apr 28:S0165-6147(25)00065-3.

doi: 10.1016/j.tips.2025.03.008. Online ahead of print.

Targeting AMPK as a potential treatment for hepatic fibrosis in MASLD

Xavier Palomer ¹, Jue-Rui Wang ¹, Claudia Escalona ¹, Siyuan Wu ¹, Walter Wahli ², Manuel Vázquez-Carrera ³

Affiliations Expand

• PMID: 40300935
• DOI: 10.1016/j.tips.2025.03.008

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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.