Anne-Marie C Overstreet, McKenzie Burge, Annette Bellar, Megan McMullen, Douglas Czarnecki, Emily Huang, Vai Pathak, Chelsea Finney, Raveena Vij, Srinivasan Dasarathy, Jaividhya Dasarathy, David Streem, Nicole Welch, Daniel Rotroff, Adam M Schmitt, Laura E Nagy, Jeannette S Messer
{"title":"Evidence that extracellular HSPB1 contributes to inflammation in alcohol-associated hepatitis","authors":"Anne-Marie C Overstreet, McKenzie Burge, Annette Bellar, Megan McMullen, Douglas Czarnecki, Emily Huang, Vai Pathak, Chelsea Finney, Raveena Vij, Srinivasan Dasarathy, Jaividhya Dasarathy, David Streem, Nicole Welch, Daniel Rotroff, Adam M Schmitt, Laura E Nagy, Jeannette S Messer","doi":"10.1101/2024.09.06.24313193","DOIUrl":null,"url":null,"abstract":"<strong>Background and aims</strong> Alcohol-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 that is rapidly increased in and released from cells experiencing stress, including hepatocytes. The goal of this study was to define the role of HSPB1 in AH pathophysiology.","PeriodicalId":501258,"journal":{"name":"medRxiv - Gastroenterology","volume":"75 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"medRxiv - Gastroenterology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.09.06.24313193","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
Background and aims Alcohol-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 that is rapidly increased in and released from cells experiencing stress, including hepatocytes. The goal of this study was to define the role of HSPB1 in AH pathophysiology.
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