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Biomolecules
Special Issues
Alcohol-Related Organ Damage: Mechanisms, Outcomes, and Treatment Modalities
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Alcohol-Related Organ Damage: Mechanisms, Outcomes, and Treatment Modalities

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 2851

Special Issue Editors

Prof. Dr. Natalia Osna

E-Mail Website
Guest Editor
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, USA
Interests: hepatitis C, B, HIV, and other viral hepatitis; alcohol-associated liver disease; innate immunity; antigen presentation; proteasome; protein posttranslational modifications; animal models for a hepatitis study; long-acting drugs
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Kusum K. Kharbanda

E-Mail Website
Guest Editor
Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68105, USA
Interests: alcohol-associated liver disease and metabolic dysfunction-associated liver disease: pathogenesis and treatment modality; methylation defects
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue has been designed to cover multiple mechanisms and treatment targets for alcohol-related organ damage, including liver, lungs, heart, kidney, brain, etc. We welcome original research articles and reviews on outcomes and co-morbidities of alcohol-associated pathologies studied experimentally or in clinical trials, with a special emphasis placed on pathogenesis-based treatment modalities.

Prof. Dr. Natalia Osna
Prof. Dr. Kusum K. Kharbanda
Guest Editors

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. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

 

Keywords

  • alcoholic liver disease (ALD)
  • steatohepatitis
  • fibrosis
  • cirhosis
  • parenhymal and non-parenhymal liver cells
  • brain
  • gut
  • lungs
  • immune responses
  • oxidative stress
  • methylation
  • viral infections
  • post-translational protein modifications
  • treatment of ALD

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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13 pages, 6803 KiB  
Article
Ethanol Disrupts the Protective Crosstalk Between Macrophages and HBV-Infected Hepatocytes
by Murali Ganesan, Anup S. Pathania, Grace Bybee, Kusum K. Kharbanda, Larisa Y. Poluektova and Natalia A. Osna
Biomolecules 2025, 15(1), 57; https://doi.org/10.3390/biom15010057 - 3 Jan 2025
Viewed by 1050
Abstract
About 296 million people worldwide are living with chronic hepatitis B viral (HBV) infection, and outcomes to end-stage liver diseases are potentiated by alcohol. HBV replicates in hepatocytes, but other liver non-parenchymal cells can sense the virus. In this study, we aimed to [...] Read more.
About 296 million people worldwide are living with chronic hepatitis B viral (HBV) infection, and outcomes to end-stage liver diseases are potentiated by alcohol. HBV replicates in hepatocytes, but other liver non-parenchymal cells can sense the virus. In this study, we aimed to investigate the regulatory effects of macrophages on HBV marker and interferon-stimulated genes (ISGs) expressions in hepatocytes. This study was performed on HBV-replicating HepG2.2.15 cells and human monocyte-derived macrophages (MDMs). We found that exposure of HepG2.2.15 cells to an acetaldehyde-generating system (AGS) increased HBV RNA, HBV DNA, and cccDNA expressions and suppressed the activation of ISGs, APOBEC3G, ISG15, and OAS1. Supernatants collected from IFNα-activated MDMs decreased HBV marker levels and induced ISG activation in AGS-treated and untreated HepG2.215 cells. These effects were reversed by exposure of MDMs to ethanol and mimicked by treatment with exosome release inhibitor GW4869. We conclude that exosome-mediated crosstalk between IFN-activated macrophages and HBV-replicating hepatocytes plays a protective role via the up-regulation of ISGs and suppression of HBV replication. However, ethanol exposure to macrophages breaks this protection. Full article
(This article belongs to the Special Issue Alcohol-Related Organ Damage: Mechanisms, Outcomes, and Treatment Modalities)
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21 pages, 10076 KiB  
Article
Late-Life Alcohol Exposure Does Not Exacerbate Age-Dependent Reductions in Mouse Spatial Memory and Brain TFEB Activity
by Hao Chen, Kaitlyn Hinz, Chen Zhang, Yssa Rodriguez, Sha Neisha Williams, Mengwei Niu, Xiaowen Ma, Xiaojuan Chao, Alexandria L. Frazier, Kenneth E. McCarson, Xiaowan Wang, Zheyun Peng, Wanqing Liu, Hong-Min Ni, Jianhua Zhang, Russell H. Swerdlow and Wen-Xing Ding
Biomolecules 2024, 14(12), 1537; https://doi.org/10.3390/biom14121537 - 30 Nov 2024
Cited by 1 | Viewed by 1243
Abstract
Alcohol consumption is believed to affect Alzheimer’s disease (AD) risk, but the contributing mechanisms are not well understood. A potential mediator of the proposed alcohol-AD connection is autophagy, a degradation pathway that maintains organelle and protein homeostasis. Autophagy is regulated through the activity [...] Read more.
Alcohol consumption is believed to affect Alzheimer’s disease (AD) risk, but the contributing mechanisms are not well understood. A potential mediator of the proposed alcohol-AD connection is autophagy, a degradation pathway that maintains organelle and protein homeostasis. Autophagy is regulated through the activity of Transcription factor EB (TFEB), which promotes lysosome and autophagy-related gene expression. The purpose of this study is to explore whether chronic alcohol consumption worsens the age-related decline in TFEB-mediated lysosomal biogenesis in the brain and exacerbates cognitive decline associated with aging. To explore the effect of alcohol on brain TFEB and autophagy, we exposed young (3-month-old) and aged (23-month-old) mice to two alcohol-feeding paradigms and assessed biochemical, transcriptome, histology, and behavioral endpoints. In young mice, alcohol decreased hippocampal nuclear TFEB staining but increased SQSTM1/p62, LC3-II, ubiquitinated proteins, and phosphorylated Tau. Hippocampal TFEB activity was lower in aged mice than it was in young mice, and Gao-binge alcohol feeding did not worsen the age-related reduction in TFEB activity. Morris Water and Barnes Maze spatial memory tasks were used to characterize the effects of aging and chronic alcohol exposure (mice fed alcohol for 4 weeks). The aged mice showed worse spatial memory acquisition in both tests. Alcohol feeding slightly impaired spatial memory in the young mice, but had little effect or even slightly improved spatial memory acquisition in the aged mice. In conclusion, aging produces greater reductions in brain autophagy flux and impairment of spatial memory than alcohol consumption. Full article
(This article belongs to the Special Issue Alcohol-Related Organ Damage: Mechanisms, Outcomes, and Treatment Modalities)
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