ReviewThe Journal of biological chemistry2020
From overnutrition to liver injury: AMP-activated protein kinase in nonalcoholic fatty liver diseases.
Review in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
55 citing papers in PubMed, 90 citations in OpenAlex.
- Pharmacodynamic effects of direct AMP kinase activation in humans with insulin resistance and non-alcoholic fatty liver disease: A phase 1b study.Cell reports. Medicine · 2021Trial
- Comparison of Physiological Responses to Plant-Protein- and Carbohydrate-Based Fishmeal Substitutes in Largemouth Bass (Animals : an open access journal from MDPI · 2026Article
- Hepassocin prevents age-related liver senescence and facilitates liver regeneration by activating AMPK.Signal transduction and targeted therapy · 2026Article
- 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
- The LKB1-AMPK pathway in NAFLD: molecular mechanisms and therapeutic implications.Journal of physiology and biochemistry · 2026Review
- Exercise-Induced Hepatic Mitochondrial Reprogramming Across Muscle-Gut-Thyroid Axes in MASLD/MASH.International journal of molecular sciences · 2026Review
- Mitophagy in Metabolic Dysfunction-Associated Fatty Liver Disease: Mechanisms, Regulatory Networks, and Therapeutic Perspectives.Inflammation · 2026Review
- Enzyme-Activated Self-Assembling Peptides Mimicking Adiponectin Multimers for Nonalcoholic Fatty Liver Disease Therapy.ACS central science · 2026Article
- Differential Effects ofNutrients · 2026Article
- Ghardaqenoids A-F: Six New Diterpenoids from the South China Sea Soft CoralMarine drugs · 2026Article
- Kinase Inhibitors for Targeted Cancer Therapy.Current topics in medicinal chemistry · 2026Review
- Hepatoprotective Formula 919 ameliorates hepatic steatosis and metabolic disturbance in NAFLD with involvement of AMPK signaling.Frontiers in pharmacology · 2026Article
- An ATF3 Inducer Ameliorates Metabolic Dysfunction-Associated Steatotic Liver Disease Through the AMPK and PKA Pathways.International journal of molecular sciences · 2025Article
- The role and function of lncRNA in ageing-associated liver diseases.RNA biology · 2025Review
- Obesity-Driven Metabolic Disorders: The Interplay of Inflammation and Mitochondrial Dysfunction.International journal of molecular sciences · 2025Review
- RXRActa pharmaceutica Sinica. B · 2025Article
- Cinnabarinic acid protects against metabolic dysfunction-associated steatohepatitis by activating aryl hydrocarbon receptor-dependent AMPK signaling.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- A Comprehensive Review of Metabolic Dysfunction-Associated Steatotic Liver Disease: Its Mechanistic Development Focusing on Methylglyoxal and Counterbalancing Treatment Strategies.International journal of molecular sciences · 2025Review
- Motor protein KIF13B orchestrates hepatic metabolism to prevent metabolic dysfunction-associated fatty liver disease.Military Medical Research · 2025Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Nonalcoholic fatty liver diseases (NAFLDs), especially nonalcoholic steatohepatitis (NASH), have become a major cause of liver transplant and liver-associated death. However, the pathogenesis of NASH is still unclear. Currently, there is no FDA-approved medication to treat this devastating disease. AMP-activated protein kinase (AMPK) senses energy status and regulates metabolic processes to maintain homeostasis. The activity of AMPK is regulated by the availability of nutrients, such as carbohydrates, lipids, and amino acids. AMPK activity is increased by nutrient deprivation and inhibited by overnutrition, inflammation, and hypersecretion of certain anabolic hormones, such as insulin, during obesity. The repression of hepatic AMPK activity permits the transition from simple steatosis to hepatocellular death; thus, activation might ameliorate multiple aspects of NASH. Here we review the pathogenesis of NAFLD and the impact of AMPK activity state on hepatic steatosis, inflammation, liver injury, and fibrosis during the transition of NAFL to NASH and liver failure.
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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 OpenQuestion graph.