ArticleActa pharmacologica Sinica2025
Rab11b promotes M1-like macrophage polarization by restraining autophagic degradation of NLRP3 in alcohol-associated liver disease.
Article in Acta pharmacologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- Macrophage ACAT1 Aggravates Alcohol-Associated Liver Disease by Inducing Mitochondrial Damage and NLRP3 Activation.Journal of gastroenterology and hepatology · 2026Article
- Genistein ameliorates non-alcoholic fatty liver disease in mice by modulating gut microbiota and hepatic macrophage polarization.Scientific reports · 2025Article
- Signs of immune dysregulation in second-trimester maternal blood RNA profiles in late-onset preeclampsia.Scientific reports · 2025Article
- Chiral gold nanoparticles manipulate osteoimmune microenvironment via macrophage autophagy for bone regeneration.Materials today. Bio · 2025Article
- Identification of Grb2 protein as a potential mediator of macrophage activation in acute pancreatitis based on bioinformatics and experimental verification.Frontiers in immunology · 2025Article
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Authors and funding
14 authors.
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Abstract
Macrophage polarization is vital to mounting a host defense or repairing tissue in various liver diseases. Excessive activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome is related to the orchestration of inflammation and alcohol-associated liver disease (ALD) pathology. Rab GTPases play critical roles in regulating vesicular transport. In this study we investigated the role of Rab11b in ALD, aiming to identify effective therapeutic targets. Here, we first demonstrated a decreased expression of Rab11b in macrophages from ALD mice. Knockdown of Rab11b by macrophage-specific adeno-associated virus can alleviate alcohol induced liver inflammation, injury and steatosis. We found that LPS and alcohol stimulation promoted Rab11b transferring from the nucleus to the cytoplasm in bone marrow-derived macrophages (BMDM) cells. Rab11b specifically activated the NLRP3 inflammasome in BMDMs and RAW264.7 cells to induce M1 macrophage polarization. Rab11b overexpression in BMDMs inhibited autophagic flux, leading to the suppression of LC3B-mediated NLRP3 degradation. We conclude that impaired Rab11b could alleviate alcohol-induced liver injury via autophagy-mediated NLRP3 degradation.
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