ReviewJournal of cellular and molecular medicine2026
Convergent Metabolic Pathways in MASH Therapeutics: An AMPK-Centric Analysis.
Review in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Palmatine ameliorates MASLD in type 2 diabetes by modulating hepatic apoptosis and inflammation.Scientific reports · 2026Article
- Calcium imbalance drives organelle network collapse and immune remodeling: novel pathogenic mechanisms in MASLD progression.Frontiers in immunology · 2026Review
- Convergent Metabolic Pathways in MASH Therapeutics: An AMPK-Centric Analysis.Journal of cellular and molecular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a leading cause of liver-related morbidity driven by systemic metabolic dysregulation. The recent approval of resmetirom and the clinical success of GLP-1 receptor agonists have heralded a new era in MASH therapy, yet a convergent understanding of the complex mechanisms of these diverse agents is lacking. This review proposes a mechanistic framework centred on the convergent signalling of AMP-activated protein kinase (AMPK), a master regulator of hepatic energy homeostasis. We examine key metabolism-based therapeutics-pioglitazone, GLP-1 receptor agonists, SGLT2 inhibitors, resmetirom and statins-to delineate how distinct upstream triggers converge on AMPK. Synthesising the latest evidence, we clearly delineate how each drug class activates AMPK either indirectly-through systemic effects like weight loss and glycemic control-or via direct actions on hepatocytes. We specifically contrast the liver-targeted action of resmetirom with the predominantly systemic effects of semaglutide and discuss the 'epigenetic lock-in' hypothesis, wherein chronic metabolic stress perpetuates the disease state. Based on this framework, we propose rational strategies for combination therapy. In conclusion, this AMPK-centric framework provides a novel lens for understanding the complex pharmacology of MASH drugs and offers a valuable clinical roadmap for personalising treatment strategies to individual patient phenotypes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.