ArticleNature communications2022
Depletion of mitochondrial methionine adenosyltransferase α1 triggers mitochondrial dysfunction in alcohol-associated liver disease.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- The Effect of Prolyl Isomerase Pin1 on the Development of Metabolic Dysfunction-Associated Steatohepatitis and a New Treatment Strategy.International journal of molecular sciences · 2026Review
- Metabolomics and Machine Learning Uncover 5'-Methylthioadenosine as a Metabolic Indicator of Mixed-Pattern Drug-Induced Liver Injury.Metabolites · 2026Article
- Article
- Revealing the spatiotemporal dynamics of methionine metabolism with a genetically encoded single-fluorophore biosensor.bioRxiv : the preprint server for biology · 2026Article
- Post-Translational Modifications of Histones and Non-Histones in Liver Disease and Traditional Chinese Medicine Treatment: A Narrative Review.Pharmacogenomics and personalized medicine · 2026Review
- Methionine Adenosyltransferase 1A and S-Adenosylmethionine in Alcohol-Associated Liver Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Distinct S-adenosylmethionine synthases link phosphatidylcholine to mitochondrial function and stress survival.PLoS biology · 2025Article
- GLS1-RNA Polymerase II Axis Mediates Glutamine-Dependent Hepatoprotective Effects on Alcoholic Liver Disease in High-Protein Diets.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Biological age construction for prediction of mortality in the Chinese population.GeroScience · 2025Article
- Posttranslational Regulation of Mammalian Sulfur Amino Acid Metabolism.International journal of molecular sciences · 2025Review
- Network analysis of cognitive function, glycemic-lipid profiles, and hepatic-renal function in individuals with diverse drinking patterns.Frontiers in endocrinology · 2025Article
- Sumoylation of methionine adenosyltransferase alpha 1 promotes mitochondrial dysfunction in alcohol-associated liver disease.Hepatology (Baltimore, Md.) · 2024Article
- Interrogating data-independent acquisition LC-MS/MS for affinity proteomics.Journal of proteins and proteomics · 2024Article
- S-Adenosylmethionine Negatively Regulates the Mitochondrial Respiratory Chain Repressor MCJ in the Liver.International journal of biological sciences · 2024Article
- PRMT1 orchestrates with SAMTOR to govern mTORC1 methionine sensing via Arg-methylation of NPRL2.Cell metabolism · 2023Article
- The intersection between alcohol-related liver disease and nonalcoholic fatty liver disease.Nature reviews. Gastroenterology & hepatology · 2023Review
- Post-translational modifications of histone and non-histone proteins in epigenetic regulation and translational applications in alcohol-associated liver disease: Challenges and research opportunities.Pharmacology & therapeutics · 2023Review
- Amino acid metabolism in health and disease.Signal transduction and targeted therapy · 2023Review
- Mitochondrial Dysfunction: At the Nexus between Alcohol-Associated Immunometabolic Dysregulation and Tissue Injury.International journal of molecular sciences · 2023Review
- Methionine restriction constrains lipoylation and activates mitochondria for nitrogenic synthesis of amino acids.Nature communications · 2023Article
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 3 countries.
Funding
Abstract
MATα1 catalyzes the synthesis of S-adenosylmethionine, the principal biological methyl donor. Lower MATα1 activity and mitochondrial dysfunction occur in alcohol-associated liver disease. Besides cytosol and nucleus, MATα1 also targets the mitochondria of hepatocytes to regulate their function. Here, we show that mitochondrial MATα1 is selectively depleted in alcohol-associated liver disease through a mechanism that involves the isomerase PIN1 and the kinase CK2. Alcohol activates CK2, which phosphorylates MATα1 at Ser114 facilitating interaction with PIN1, thereby inhibiting its mitochondrial localization. Blocking PIN1-MATα1 interaction increased mitochondrial MATα1 levels and protected against alcohol-induced mitochondrial dysfunction and fat accumulation. Normally, MATα1 interacts with mitochondrial proteins involved in TCA cycle, oxidative phosphorylation, and fatty acid β-oxidation. Preserving mitochondrial MATα1 content correlates with higher methylation and expression of mitochondrial proteins. Our study demonstrates a role of CK2 and PIN1 in reducing mitochondrial MATα1 content leading to mitochondrial dysfunction in alcohol-associated liver disease.
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