ReviewWorld journal of gastroenterology2010
AMPK-associated signaling to bridge the gap between fuel metabolism and hepatocyte viability.
Review in World journal of gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Mitochondria transfer in tissue homeostasis and diseases.International journal of biological sciences · 2026Review
- Cranberry improves metabolic syndrome-related organ dysfunction in rats by modulating AMPK/SREBP1, ROCK1 and TGF-β1.Scientific reports · 2025Article
- Crosstalk between lipid metabolism and EMT: emerging mechanisms and cancer therapy.Molecular and cellular biochemistry · 2025Article
- Tirzepatide alleviates non-alcoholic fatty liver disease by regulating lipid metabolism through activation of the AMPK/NF-κB signaling pathway.American journal of translational research · 2025Article
- Coordination of AMPK and YAP byInternational journal of molecular sciences · 2022Article
- A bioactive component ofToxicology research · 2022Article
- Ketone bodies: from enemy to friend and guardian angel.BMC medicine · 2021Review
- Interleukin-22 drives a metabolic adaptive reprogramming to maintain mitochondrial fitness and treat liver injury.Theranostics · 2020Article
- Effect of resveratrol on non-alcoholic fatty liver disease.Experimental and therapeutic medicine · 2019Article
- GADD45α alleviates acetaminophen-induced hepatotoxicity by promoting AMPK activation.Cellular and molecular life sciences : CMLS · 2019Article
- AMPK: Potential Therapeutic Target for Ischemic Stroke.Theranostics · 2018Review
- Enhanced autophagy contributes to protective effects of IL-22 against acetaminophen-induced liver injury.Theranostics · 2018Article
- Hypothermic machine perfusion with metformin-University of Wisconsin solution forWorld journal of gastroenterology · 2017Article
- AMPK activation by liquiritigenin inhibited oxidative hepatic injury and mitochondrial dysfunction induced by nutrition deprivation as mediated with induction of farnesoid X receptor.European journal of nutrition · 2017Article
- Phytochemicals in Ischemic Stroke.Neuromolecular medicine · 2016Review
- Resveratrol Inhibition of Cellular Respiration: New Paradigm for an Old Mechanism.International journal of molecular sciences · 2016Review
- A load of mice to hypergravity causes AMPKα repression with liver injury, which is overcome by preconditioning loads via Nrf2.Scientific reports · 2015Article
- Enhanced Production of Adenosine Triphosphate by Pharmacological Activation of Adenosine Monophosphate-Activated Protein Kinase Ameliorates Acetaminophen-Induced Liver Injury.Molecules and cells · 2015Article
- Effects of long-term treatment with quercetin on cognition and mitochondrial function in a mouse model of Alzheimer's disease.Neurochemical research · 2014Article
- Effects of resveratrol in experimental and clinical non-alcoholic fatty liver disease.World journal of hepatology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adenosine monophosphate-activated protein kinase (AMPK) and p70 ribosomal S6 kinase-1 pathway may serve as a key signaling flow that regulates energy metabolism; thus, this pathway becomes an attractive target for the treatment of liver diseases that result from metabolic derangements. In addition, AMPK emerges as a kinase that controls the redox-state and mitochondrial function, whose activity may be modulated by antioxidants. A close link exists between fuel metabolism and mitochondrial biogenesis. The relationship between fuel metabolism and cell survival strongly implies the existence of a shared signaling network, by which hepatocytes respond to challenges of external stimuli. The AMPK pathway may belong to this network. A series of drugs and therapeutic candidates enable hepatocytes to protect mitochondria from radical stress and increase cell viability, which may be associated with the activation of AMPK, liver kinase B1, and other molecules or components. Consequently, the components downstream of AMPK may contribute to stabilizing mitochondrial membrane potential for hepatocyte survival. In this review, we discuss the role of the AMPK pathway in hepatic energy metabolism and hepatocyte viability. This information may help identify ways to prevent and/or treat hepatic diseases caused by the metabolic syndrome. Moreover, clinical drugs and experimental therapeutic candidates that directly or indirectly modulate the AMPK pathway in distinct manners are discussed here with particular emphasis on their effects on fuel metabolism and mitochondrial function.
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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.