ArticleNature medicine2017
Tmbim1 is a multivesicular body regulator that protects against non-alcoholic fatty liver disease in mice and monkeys by targeting the lysosomal degradation of Tlr4.
Article in Nature medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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71 citing papers in PubMed, 149 citations in OpenAlex.
- Bayesian Genome-Wide Association Study of Feed Efficiency Traits in Pigs.Animals : an open access journal from MDPI · 2026Article
- A tale of dual role: HECT‑type E3 ubiquitin ligase mechanisms in liver diseases (Review).International journal of molecular medicine · 2026Review
- Th17-related genes PGAP1 and TMBIM1 serve as potential diagnostic and predictive biomarkers in systemic sclerosis: bioinformatic identification and murine model validation.Clinical rheumatology · 2026Article
- Loss of Epithelial Homeostasis Driven by TMBIM1 Depletion via E-Cadherin Junction Disassembly.International journal of molecular sciences · 2026Article
- Gut microbiota and the gut-liver axis in MASLD: mechanisms, immune regulation and therapeutic opportunities.Frontiers in pharmacology · 2026Review
- Fas apoptotic inhibitor molecule 2 mitigates metabolic dysfunction-associated fatty liver disease through autophagic CRTC2 degradation.Experimental & molecular medicine · 2025Article
- Ubiquitination and ubiquitin-like modifications in metabolic dysfunction-associated steatotic liver disease: mechanisms and implications.BMB reports · 2025Review
- Liver immunology: Biological role and clinical significance.World journal of hepatology · 2025Review
- Phosphorylated IRF3 promotes GSDME-mediated pyroptosis through RIPK1/FADD/caspase-8 complex formation during mitotic arrest in ovarian cancer.Cell communication and signaling : CCS · 2025Article
- Gene-based therapies for steatotic liver disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- TMBIM1 promotes epithelial mesenchymal transition by accelerating autophagic degradation of E-cadherin in glioblastoma.Scientific reports · 2025Article
- Identification of Critical Molecular Pathways Induced by HDAC11 Overexpression in Cardiac Mesenchymal Stem Cells.Biomolecules · 2025Article
- The NbInternational journal of nanomedicine · 2025Article
- The role of ubiquitination and deubiquitination in the pathogenesis of non-alcoholic fatty liver disease.Frontiers in immunology · 2025Review
- The secrets of menstrual blood: emerging frontiers from diagnostic tools to stem cell therapies.Frontiers in cell and developmental biology · 2025Review
- Progress in the Study of Animal Models of Metabolic Dysfunction-Associated Steatotic Liver Disease.Nutrients · 2024Review
- The impact of exercise on gene regulation in association with complex trait genetics.Nature communications · 2024Article
- MicroRNA-582-3p knockdown alleviates non-alcoholic steatohepatitis by altering the gut microbiota composition and moderating TMBIM1.Irish journal of medical science · 2024Article
- Common molecular basis for MASH and hepatitis C revealed via systems biology approach.Frontiers in oncology · 2024Article
- Annexin A5 Derived from Cell-free Fat Extract Attenuates Osteoarthritis via Macrophage Regulation.International journal of biological sciences · 2024Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic steatohepatitis (NASH) is an increasingly prevalent liver pathology that can progress from non-alcoholic fatty liver disease (NAFLD), and it is a leading cause of cirrhosis and hepatocellular carcinoma. There is currently no pharmacological therapy for NASH. Defective lysosome-mediated protein degradation is a key process that underlies steatohepatitis and a well-recognized drug target in a variety of diseases; however, whether it can serve as a therapeutic target for NAFLD and NASH remains unknown. Here we report that transmembrane BAX inhibitor motif-containing 1 (TMBIM1) is an effective suppressor of steatohepatitis and a previously unknown regulator of the multivesicular body (MVB)-lysosomal pathway. Tmbim1 expression in hepatocytes substantially inhibited high-fat diet-induced insulin resistance, hepatic steatosis and inflammation in mice. Mechanistically, Tmbim1 promoted the lysosomal degradation of toll-like receptor 4 by cooperating with the ESCRT endosomal sorting complex to facilitate MVB formation, and the ubiquitination of Tmbim1 by the E3 ubiquitin ligase Nedd4l was required for this process. We also found that overexpression of Tmbim1 in the liver effectively inhibited a severe form of NAFLD in mice and NASH progression in monkeys. Taken together, these findings could lead to the development of promising strategies to treat NASH by targeting MVB regulators to properly orchestrate the lysosome-mediated protein degradation of key mediators of the disease.
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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.