ArticleNature communications2022
TFEB regulates sulfur amino acid and coenzyme A metabolism to support hepatic metabolic adaptation and redox homeostasis.
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 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Liver-to-kidney apolipoprotein J trans-accumulation exacerbates diabetic renal injury by disrupting TFEB-mediated lipid homeostasis.Diabetologia · 2026Article
- Amino Acid Metabolism in Health and Disease.MedComm · 2026Review
- Comparison of Liquid Chromatography- and Nano-Electrospray Ionization-Mass Spectrometry Approaches for Single-Cell Metabolomics.Analytical chemistry · 2026Article
- Hepatocyte and adipocyte CDO1-mediated intracellular cysteine catabolism differentially modulates diet-induced obesity and fatty liver in mice.bioRxiv : the preprint server for biology · 2025Article
- Ubiquitination of TFEB increased intestinal permeability to aggravate metabolic dysfunction-associated steatohepatitis.Hepatology (Baltimore, Md.) · 2025Article
- Amino acid restriction in obesity management: Inducing energy discharge.Acta pharmaceutica Sinica. B · 2025Article
- Role of amino acids in the regulation of hepatic gluconeogenesis and lipogenesis in metabolic dysfunctionassociated steatotic liver disease.Clinical and molecular hepatology · 2025Review
- HLH-30/TFEB Rewires the Chaperone Network to Promote Proteostasis Upon Perturbations to the Coenzyme A and Iron-Sulfur Cluster Biosynthesis Pathways.Aging cell · 2025Article
- Transcription factor EB (TFEB) activity increases resistance of TNBC stem cells to metabolic stress.Life science alliance · 2025Article
- Bile acid sequestrant inhibits gluconeogenesis via inducing hepatic cysteine dioxygenase type 1 to reduce cysteine availability.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Bile acids regulation of cellular stress responses in liver physiology and diseases.eGastroenterology · 2024Article
- Deletion of hepatocyte cysteine dioxygenase type 1, a bile acid repressed gene, enhances glutathione synthesis and ameliorates acetaminophen hepatotoxicity.Biochemical pharmacology · 2024Article
- Regulation of antioxidants in cancer.Molecular cell · 2024Review
- Article
- Sulfur-Element containing metabolic pathways in human health and crosstalk with the microbiome.Biochemistry and biophysics reports · 2023Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Fatty liver is a highly heterogenous condition driven by various pathogenic factors in addition to the severity of steatosis. Protein insufficiency has been causally linked to fatty liver with incompletely defined mechanisms. Here we report that fatty liver is a sulfur amino acid insufficient state that promotes metabolic inflexibility via limiting coenzyme A availability. We demonstrate that the nutrient-sensing transcriptional factor EB synergistically stimulates lysosome proteolysis and methionine adenosyltransferase to increase cysteine pool that drives the production of coenzyme A and glutathione, which support metabolic adaptation and antioxidant defense during increased lipid influx. Intriguingly, mice consuming an isocaloric protein-deficient Western diet exhibit selective hepatic cysteine, coenzyme A and glutathione deficiency and acylcarnitine accumulation, which are reversed by cystine supplementation without normalizing dietary protein intake. These findings support a pathogenic link of dysregulated sulfur amino acid metabolism to metabolic inflexibility that underlies both overnutrition and protein malnutrition-associated fatty liver development.
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Registered trials
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