ReviewBiomolecules & therapeutics2025
New Insights into AMPK, as a Potential Therapeutic Target in Metabolic Dysfunction-Associated Steatotic Liver Disease and Hepatic Fibrosis.
Review in Biomolecules & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The Role of the Gut Microbiome in Clinical Outcomes of Colorectal Cancer: A Systematic Review (2020-2025).Oncology research · 2026Pooled it
- Bioactives and exercise synergize to modulate AMPK and inflammation.Frontiers in immunology · 2025Pooled it
- Vanadium(IV)-chlorodipicolinate alleviates hepatic steatosis via the AMPK/PGC-1α/CPT1a axis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Review
- Chronic infection and metabolic stress: a converging axis driving hypertension and metabolic dysfunction-associated steatotic liver disease outcomes.American journal of hypertension · 2026Review
- Autophagy in MASLD: A Metabolic and Precision Medicine Perspective.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- AMPK Therapy-A Little Goes A Long Way.Cells · 2026Review
- Adipose Tissue Browning in MASLD and Its Molecular Mechanisms and Metabolic Crosstalk.Current obesity reports · 2026Review
- Abelmoschus manihot Polysaccharides Target the AMPK/Nrf2/HO-1 Signalling Pathway to Inhibit Macrophage M1 Polarisation and Hepatic Stellate Cell Activation Improving Liver Fibrosis in Mice.Journal of cellular and molecular medicine · 2026Article
- Management of MASLD/MASH: challenges, innovations, and the future of patient-centered care in Japan.Journal of gastroenterology · 2026Review
- Comparative study on the protective effects of Silybum marianum L. seeds and leaves against nickel chloride induced anemia, liver and kidney injury: an in vivo and in silico approach.Scientific reports · 2026Article
- GLP-1 receptor agonists as multisystem therapies: from glycemic control to cardiorenal, neuroimmune, and metabolic disease.Diabetology & metabolic syndrome · 2026Review
- Review
- Advances in natural compounds modulating autophagy for the therapeutic intervention of heart failure.Molecular and cellular biochemistry · 2026Review
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- Dose-response relationships of normal blood lipid levels in metabolic and endocrine diseases: mechanistic similarities, differences, and functional insights.Frontiers in endocrinology · 2026Review
- Exercise and cold exposure as dual physiological stressors in MASLD: AMPK-mediated metabolic adaptation and interorgan crosstalk.Frontiers in physiology · 2026Review
- Navigating the New Therapeutic Landscape: Innovative Strategies for Overcoming Resistance and Degeneration.Biomolecules & therapeutics · 2026Article
- Beyond Bioenergetics: Emerging Roles of Mitochondrial Fatty Acid Oxidation in Stress Response and Aging.Cells · 2025Review
- Nicorandil attenuates thioacetamide induced liver fibrosis via AMPK, SIRT1 and HIF1α mediated cellular energy homeostasis.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AMP-activated protein kinase (AMPK) activators have garnered significant attention for their potential to prevent the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) into liver fibrosis and to fundamentally improve liver function. The broad spectrum of pathways regulated by AMPK activators makes them promising alternatives to conventional liver replacement therapies and the limited pharmacological treatments currently available. In this study, we aim to illustrate the newly detailed multiple mechanisms of MASLD progression based on the multiple-hit hypothesis. This model posits that impaired lipid metabolism, combined with insulin resistance and metabolic imbalance, initiates inflammatory cascades, gut dysbiosis, and the accumulation of toxic metabolites, ultimately promoting fibrosis and accelerating MASLD progression to irreversible hepatocellular carcinoma (HCC). AMPK plays a multifaceted protective role against these pathological conditions by regulating several key downstream signaling pathways. It regulates biological effectors critical to metabolic and inflammatory responses, such as SIRT1, Nrf2, mTOR, and TGF-β, through complex and interrelated mechanisms. Due to these intricate connections, AMPK's role is pivotal in managing metabolic and inflammatory disorders. In this review, we demonstrate the specific roles of AMPK and its related pathways. Several agents directly activate AMPK by binding as agonists, while some others indirectly activate AMPK by modulating upstream molecules, including adiponectin, LKB1, and the AMP: ATP ratio. As AMPK activators can target each stage of MASLD progression, the development of AMPK activators offers immense potential to expand therapeutic strategies for liver diseases such as MASH, MASLD, and liver fibrosis.
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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.