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The Pathogenesis of Alcohol-Associated Hepatitis and Its Therapies
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The Pathogenesis of Alcohol-Associated Hepatitis and Its Therapies

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 264

Special Issue Editor

Dr. Mrigya Babuta

E-Mail Website
Guest Editor
Harvard Medical School, Boston, MA, USA
Interests: liver

Special Issue Information

Dear Colleagues,

Alcohol-associated liver disease (ALD) is a multifactorial liver disease caused by heavy alcohol consumption and characterized by steatosis, hepatitis, fibrosis/cirrhosis, and enhanced risk of hepatocellular carcinoma. Alcohol-associated hepatitis (AH) is a pathological condition caused by an excessive intake of alcohol and displays an acute liver injury and a high mortality rate >30% within 180 days after diagnosis. Corticosteroid treatment is the standard therapy for alcoholic hepatitis, and its minimal efficacy necessitates the exploration of new, therapeutic options for treating alcoholic hepatitis patients.

The pathogenesis of AH involves hepatocyte damage, macrophage activation, the release of proinflammatory cytokines, and elevated levels of circulating exosomes in the plasma. Systemic inflammation, infection, in combination with multiorgan failure results in poorer outcomes in AH patients.

This Special Issue of the International Journal of Molecular Sciences will focus on recent developments in the pathogenesis of Alcohol-associated Hepatitis as well as new insights into the therapies for AH. This special issue welcomes researchers to contribute original research articles, review articles, and systemic reviews. 

Dr. Mrigya Babuta
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • alcohol-associted hepatitis
  • acute kidney injury
  • hepatic encephalopathy
  • adaptive immune response
  • innate immune response
  • neutrophilia

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Published Papers (1 paper)

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Research

12 pages, 1890 KiB  
Article
Hepatic Proteomic Changes Associated with Liver Injury Caused by Alcohol Consumption in Fpr2−/− Mice
by Josiah E. Hardesty, Jeffrey B. Warner, Daniel W. Wilkey, Brett S. Phinney, Michelle R. Salemi, Michael L. Merchant, Craig J. McClain, Dennis R. Warner and Irina A. Kirpich
Int. J. Mol. Sci. 2024, 25(18), 9807; https://doi.org/10.3390/ijms25189807 - 11 Sep 2024
Viewed by 86
Abstract
Alcohol-associated liver disease (ALD) is a prevalent medical problem with limited effective treatment strategies. Although many biological processes contributing to ALD have been elucidated, a complete understanding of the underlying mechanisms is still lacking. The current study employed a proteomic approach to identify [...] Read more.
Alcohol-associated liver disease (ALD) is a prevalent medical problem with limited effective treatment strategies. Although many biological processes contributing to ALD have been elucidated, a complete understanding of the underlying mechanisms is still lacking. The current study employed a proteomic approach to identify hepatic changes resulting from ethanol (EtOH) consumption and the genetic ablation of the formyl peptide receptor 2 (FPR2), a G-protein coupled receptor known to regulate multiple signaling pathways and biological processes, in a mouse model of ALD. Since previous research from our team demonstrated a notable reduction in hepatic FPR2 protein levels in patients with alcohol-associated hepatitis (AH), the proteomic changes in the livers of Fpr2−/− EtOH mice were compared to those observed in patients with AH in order to identify common hepatic proteomic alterations. Several pathways linked to exacerbated ALD in Fpr2−/− EtOH mice, as well as hepatic protein changes resembling those found in patients suffering from AH, were identified. These alterations included decreased levels of coagulation factors F2 and F9, as well as reduced hepatic levels of glutamate-cysteine ligase catalytic subunit (GCLC) and total glutathione in Fpr2−/− EtOH compared to WT EtOH mice. In conclusion, the data suggest that FPR2 may play a regulatory role in hepatic blood coagulation and the antioxidant system, both in a pre-clinical model of ALD and in human AH, however further experiments are required to validate these findings. Full article
(This article belongs to the Special Issue The Pathogenesis of Alcohol-Associated Hepatitis and Its Therapies)
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