Please use this identifier to cite or link to this item: https://dspace.iiti.ac.in/handle/123456789/14575
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dc.contributor.authorPatidar, Pramoden_US
dc.contributor.authorBharti, Shreyaen_US
dc.contributor.authorBaig, Mirza Saqiben_US
dc.date.accessioned2024-10-08T11:09:22Z-
dc.date.available2024-10-08T11:09:22Z-
dc.date.issued2024-
dc.identifier.citationPatidar, P., Hirani, N., Bharti, S., & Baig, M. S. (2024). Key regulators of hepatic stellate cell activation in alcohol liver Disease: A comprehensive review. International Immunopharmacology. Scopus. https://doi.org/10.1016/j.intimp.2024.112938en_US
dc.identifier.issn1567-5769-
dc.identifier.otherEID(2-s2.0-85201467450)-
dc.identifier.urihttps://doi.org/10.1016/j.intimp.2024.112938-
dc.identifier.urihttps://dspace.iiti.ac.in/handle/123456789/14575-
dc.description.abstractAlcoholic liver disease (ALD) is a broad category of disorders that begin with liver injury, lead to liver fibrosis, and ultimately conclude in alcohol-induced liver cirrhosis, the most chronic and irreversible liver damage. Liver fibrosis (LF) is a common pathological characteristic observed in most chronic liver inflammatory conditions that involve prolonged inflammation. In this review, we have summarized ethanol-mediated hepatic stellate cell (HSCs) activation and its role in liver fibrosis progression. We highlight important molecular mechanisms that are modulated by ethanol, play a role in the activation of HSCs and the progression of liver fibrosis and identifying potential targets to ameliorate liver fibrosis. © 2024en_US
dc.language.isoenen_US
dc.publisherElsevier B.V.en_US
dc.sourceInternational Immunopharmacologyen_US
dc.subjectAlcoholic Liver Disease (ALD)en_US
dc.subjectChronic Liver Disease (CLD)en_US
dc.subjectHepatic Stellate Cells (HSCs)en_US
dc.subjectLiver Fibrosis (LF)en_US
dc.titleKey regulators of hepatic stellate cell activation in alcohol liver Disease: A comprehensive reviewen_US
dc.typeReviewen_US
Appears in Collections:Department of Biosciences and Biomedical Engineering

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