ArticleHepatology communications2025
Evidence that extracellular HSPB1 contributes to inflammation in alcohol-associated hepatitis.
Article in Hepatology communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Natural Alkaloids Against Liver Injury: Mechanistic Insights and Multi-Target Therapeutic Potential.Biomolecules · 2026Review
- Machine Learning and Experimental Validation Identified Ferroptosis Signature and Innovative Biomarkers (ESR1 and GSTZ1) in Liver Fibrosis.Journal of inflammation research · 2024Article
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Abstract
backgroundAlcohol-associated hepatitis (AH) is the most life-threatening form of alcohol-associated liver disease (ALD). AH is characterized by severe inflammation attributed to increased levels of ethanol, microbes or microbial components, and damage-associated molecular pattern (DAMP) molecules in the liver. HSPB1 [Heat Shock Protein Family B (Small) Member 1; also known as Hsp25/27] is a DAMP released from stressed cells, including hepatocytes. The goal of this study was to define the role of HSPB1 in AH pathophysiology.
methodsSerum HSPB1 was measured in a retrospective study of 184 healthy controls (HCs), heavy alcohol consumers (HA), patients with alcohol-associated cirrhosis (AC), and patients with AH recruited from major hospital centers.HSPB1 was also evaluated in liver tissue from HC and AH patients, existing RNA-seq data from ALD patient liver and monocytes, and livers from mice fed a Lieber-DeCarli diet. Cellular models of hepatocyte and macrophage interactions were used to evaluate the role of HSPB1 in inflammation during AH.
resultsCirculating HSPB1 was significantly increased in AH patients, and levels positively correlated with disease-severity scores. HSPB1 was also increased in the livers of patients with severe AH and ethanol-fed mice. In cellular models, ethanol-stressed hepatocytes released HSPB1, which then triggered TNFα-mediated inflammation in macrophages. Anti-HSPB1 antibody prevented TNFα release from macrophages exposed to media conditioned by ethanol-stressed hepatocytes.
conclusionsOur findings support investigation of HSPB1 as both a biomarker and therapeutic target in ALD. Furthermore, this work demonstrates that anti-HSPB1 antibody is a rational approach to targeting HSPB1 with the potential to block inflammation and protect hepatocytes, without inactivating host defense.
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