ArticleCell metabolism2024
Myeloid beta-arrestin 2 depletion attenuates metabolic dysfunction-associated steatohepatitis via the metabolic reprogramming of macrophages.
Article in Cell metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 2026Review
- Offense and defense: itaconate mediates bidirectional immune regulation of host-bacteria interaction.Journal of biomedical science · 2026Review
- Metabolic Pathways Linking Atherosclerotic Cardiovascular Disease With Metabolic Dysfunction-Associated Steatotic Liver Disease.Current atherosclerosis reports · 2026Review
- Arrb2 in hepatocytes promotes M2 macrophage polarization, ameliorates hepatic ischemia-reperfusion injury through upregulating metabolite 6-ketoLCA.Hepatology communications · 2026Article
- N6-methyladenosine-mediated up-regulation of ARRB2 regulates intrahepatic cholangiocarcinoma malignant progression and pemigatinib resistance through MAPK and Hippo signaling pathways.Cell death & disease · 2026Article
- Pomolic acid alleviates CClScientific reports · 2026Article
- Supplementation of L-aspartate corrects MASLD and MASH in mice by inhibiting platelet-hepatocyte interaction-mediated mitochondrial fragmentation via the ATP-P2X7-NEK7-DRP1 axis.Experimental & molecular medicine · 2026Article
- Dysregulation of the AMPK-SREBP1-FASN axis in MASLD: driving a vicious cycle of lipotoxicity and metabolic-immune crosstalk.Lipids in health and disease · 2026Review
- Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation.Biology · 2026Review
- pH-responsive and dual-dynamically crosslinked metal-phenolic hydrogel for synergistic macrophage and Th17/Treg reprogramming in diabetic wounds.Journal of nanobiotechnology · 2026Article
- GPR43 alleviates LPS-induced acute lung injury by inhibiting NLRP3 inflammasome activation via β-arrestin 2.Biology direct · 2026Article
- Spatial immune dysregulation in MASLD: integration of lobular zoning, metabolism and immune function.Frontiers in immunology · 2026Review
- Revisiting macrophage metabolic reprogramming in metabolic dysfunction-associated steatotic liver disease: mechanisms, regulation, and therapeutic breakthroughs.Frontiers in immunology · 2026Review
- Article
- Effects of glucagon-like peptide-1 receptor agonists on patients with metabolic dysfunction-associated steatohepatitis: protocol for a systematic review and sequential meta-analysis.Systematic reviews · 2025Article
- MPPMolecular biology reports · 2025Article
- The Endocannabinoid System in Human Disease: Molecular Signaling, Receptor Pharmacology, and Therapeutic Innovation.International journal of molecular sciences · 2025Review
- Immunopathogenic mechanisms and immunoregulatory therapies in MASLD.Cellular & molecular immunology · 2025Review
- Identification of foam cell like M2 macrophages, AEBP1 biomarkers, and resveratrol as potential therapeutic in MASLD using Ecotyper and WGCNA.Scientific reports · 2025Article
- Neuro-immune cross-talk in cancer.Nature reviews. Cancer · 2025Review
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Authors and funding
21 authors.
Funding
Abstract
Macrophage-mediated inflammation has been implicated in the pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH); however, the immunometabolic program underlying the regulation of macrophage activation remains unclear. Beta-arrestin 2, a multifunctional adaptor protein, is highly expressed in bone marrow tissues and macrophages and is involved in metabolism disorders. Here, we observed that β-arrestin 2 expression was significantly increased in the liver macrophages and circulating monocytes of patients with MASH compared with healthy controls and positively correlated with the severity of metabolic dysfunction-associated steatotic liver disease (MASLD). Global or myeloid Arrb2 deficiency prevented the development of MASH in mice. Further study showed that β-arrestin 2 acted as an adaptor protein and promoted ubiquitination of immune responsive gene 1 (IRG1) to prevent increased itaconate production in macrophages, which resulted in enhanced succinate dehydrogenase activity, thereby promoting the release of mitochondrial reactive oxygen species and M1 polarization. Myeloid β-arrestin 2 depletion may be a potential approach for MASH.
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