ArticleNature communications2021
GP73 is a TBC-domain Rab GTPase-activating protein contributing to the pathogenesis of non-alcoholic fatty liver disease without obesity.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- GP73-dependent regulation of exosome biogenesis promotes colorectal cancer liver metastasis.Molecular cancer · 2025Article
- Risk factor analysis and predictive model construction of lean MAFLD: a cross-sectional study of a health check-up population in China.European journal of medical research · 2025Review
- Diagnostic Accuracy of Golgi Protein 73 (GP73) for Liver Fibrosis Staging in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Scoping Review and Cohort Study.Diagnostics (Basel, Switzerland) · 2025Article
- Extracellular vesicle-mediated approaches for the diagnosis and therapy of MASLD: current advances and future prospective.Lipids in health and disease · 2025Review
- GP73 reinforces cytotoxic T-cell function by regulating HIF-1α and increasing antitumor efficacy.Journal for immunotherapy of cancer · 2025Article
- Advances in the Use of Metformin for Liver Disease.Current medicinal chemistry · 2025Review
- Restoring metabolic flexibility: targeting organelle interaction networks in the pathogenesis and therapy of MASLD.Frontiers in cell and developmental biology · 2025Review
- Increase in bile acids after sleeve gastrectomy improves metabolism by activating GPBAR1 to increase cAMP in mice with nonalcoholic fatty liver disease.Immunity, inflammation and disease · 2024Article
- Deficiency of ASGR1 promotes liver injury by increasing GP73-mediated hepatic endoplasmic reticulum stress.Nature communications · 2024Article
- VLDL Biogenesis and Secretion: It Takes a Village.Circulation research · 2024Review
- Article
- Golgi protein 73: the driver of inflammation in the immune and tumor microenvironment.Frontiers in immunology · 2024Review
- Clinical Characteristics, Risk Factors, and Predictors of Nonobese Fatty Liver Disease: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Hepatitis B virus promotes hepatocellular carcinoma development by activating GP73 to repress the innate immune response.Infectious agents and cancer · 2022Article
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Authors and funding
33 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prevalence of non-obese nonalcoholic fatty liver disease (NAFLD) is increasing worldwide with unclear etiology and pathogenesis. Here, we show GP73, a Golgi protein upregulated in livers from patients with a variety of liver diseases, exhibits Rab GTPase-activating protein (GAP) activity regulating ApoB export. Upon regular-diet feeding, liver-GP73-high mice display non-obese NAFLD phenotype, characterized by reduced body weight, intrahepatic lipid accumulation, and gradual insulin resistance development, none of which can be recapitulated in liver-GAP inactive GP73-high mice. Common and specific gene expression signatures associated with GP73-induced non-obese NAFLD and high-fat diet (HFD)-induced obese NAFLD are revealed. Notably, metformin inactivates the GAP activity of GP73 and alleviates GP73-induced non-obese NAFLD. GP73 is pathologically elevated in NAFLD individuals without obesity, and GP73 blockade improves whole-body metabolism in non-obese NAFLD mouse model. These findings reveal a pathophysiological role of GP73 in triggering non-obese NAFLD and may offer an opportunity for clinical intervention.
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