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Cells
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Alcohol-Induced Tissue and Organ Damage: Mechanisms and Therapeutic Approaches
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Alcohol-Induced Tissue and Organ Damage: Mechanisms and Therapeutic Approaches

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: closed (10 October 2023) | Viewed by 8053

Special Issue Editor

Prof. Dr. Wayne Carver

E-Mail Website
Guest Editor
Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29209, USA
Interests: fibrosis; extracellular matrix; fibroblast activation; integrins; cardiovascular disease; alcohol abuse; decellularization; tissue engineering
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alcohol is a psychoactive substance that continues to be widely used in many cultures. Acute or chronic consumption of excessive levels of alcohol contributes to numerous pathological conditions, resulting in enormous economic and social burden. Alcohol affects most organs and organ systems and chronic abuse of alcohol can result in alcoholic hepatitis and liver cirrhosis, pancreatitis, cardiomyopathy, brain damage, cancer, immune system defects, fetal abnormalities and other conditions. According to the World Health Organization, three million deaths, or over 5 percent of deaths worldwide, result annually from the harmful use of alcohol. Alcohol is able to enter all cells and the response to alcohol is affected by a variety of genetic and environmental factors. Alcohol and its metabolites alter cellular functions through changes at the levels of nucleic acids, proteins and general metabolism resulting in deleterious tissue remodeling. Emerging evidence indicates that some common mechanisms may underlie alcohol-induced tissue damage including oxidative stress, inflammation and apoptotic pathways. A better understanding of the diverse molecular and cellular mechanisms underlying tissue remodeling in response to excessive alcohol consumption will hopefully provide novel therapeutic approaches to treat alcohol-induced tissue damage. 

The aim of this Special Issue of Cells is to present the current knowledge of alcohol-induced tissue damage through thorough reviews and primary research articles. Manuscripts broadly focused on the effects of alcohol on diverse systems and the various cellular and molecular mechanisms of this response are invited. Translational studies, including those focused on novel therapeutics, are particularly welcome.

Prof. Dr. Wayne Carver
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. Cells is an international peer-reviewed open access semimonthly 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

  • alcohol abuse
  • alcohol tissue damage
  • ethanol
  • alcohol misuse
  • alcohol organ damage

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Published Papers (4 papers)

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Research

19 pages, 2579 KiB  
Article
Abstinence Restores Cardiac Function in Mice with Established Alcohol-Induced Cardiomyopathy
by Joshua M. Edavettal, Nicholas R. Harris, Sarah E. Cohen, Janos Paloczi, Bysani Chandrasekar and Jason D. Gardner
Cells 2023, 12(24), 2783; https://doi.org/10.3390/cells12242783 - 7 Dec 2023
Cited by 1 | Viewed by 1342
Abstract
Alcohol-induced cardiomyopathy (ACM) has a poor prognosis with up to a 50% chance of death within four years of diagnosis. There are limited studies investigating the potential of abstinence for promoting repair after alcohol-induced cardiac damage, particularly in a controlled preclinical study design. [...] Read more.
Alcohol-induced cardiomyopathy (ACM) has a poor prognosis with up to a 50% chance of death within four years of diagnosis. There are limited studies investigating the potential of abstinence for promoting repair after alcohol-induced cardiac damage, particularly in a controlled preclinical study design. Here, we developed an exposure protocol that led to significant decreases in cardiac function in C57BL6/J mice within 30 days; dP/dt max decreased in the mice fed alcohol for 30 days (8054 ± 664.5 mmHg/s compared to control mice: 11,188 ± 724.2 mmHg/s, p < 0.01), and the dP/dt min decreased, as well (−7711 ± 561 mmHg/s compared to control mice: −10,147 ± 448.2 mmHg/s, p < 0.01). Quantitative PCR was used to investigate inflammatory and fibrotic biomarkers, while histology was used to depict overt changes in cardiac fibrosis. We observed a complete recovery of function after abstinence (dP/dt max increased from 8054 ± 664 mmHg/s at 30 days to 11,967 ± 449 mmHg/s after abstinence, p < 0.01); further, both inflammatory and fibrotic biomarkers decreased after abstinence. These results lay the groundwork for future investigation of the molecular mechanisms underlying recovery from alcohol-induced damage in the heart. Full article
(This article belongs to the Special Issue Alcohol-Induced Tissue and Organ Damage: Mechanisms and Therapeutic Approaches)
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13 pages, 12708 KiB  
Article
mTOR Inhibitor Rapalink-1 Prevents Ethanol-Induced Senescence in Endothelial Cells
by Huakang Zhou, Xuanchen Li, Majeed Rana, Jan Frederick Cornelius, Dilaware Khan and Sajjad Muhammad
Cells 2023, 12(22), 2609; https://doi.org/10.3390/cells12222609 - 11 Nov 2023
Cited by 6 | Viewed by 2307
Abstract
The cardiovascular risk factors, including smoking, ethanol, and oxidative stress, can induce cellular senescence. The senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase (MMPs). These pro-inflammatory molecules and MMPs promote the infiltration and accumulation of inflammatory cells in [...] Read more.
The cardiovascular risk factors, including smoking, ethanol, and oxidative stress, can induce cellular senescence. The senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase (MMPs). These pro-inflammatory molecules and MMPs promote the infiltration and accumulation of inflammatory cells in the vascular tissue, exacerbating vascular tissue inflammation. MMPs damage vascular tissue by degenerating the extracellular matrix. Consequently, these cellular and molecular events promote the initiation and progression of cardiovascular diseases. We used Rapalink-1, an mTOR inhibitor, to block ethanol-induced senescence. Rapalink-1 inhibited oxidative-stress-induced DNA damage and senescence in endothelial cells exposed to ethanol. It attenuated the relative protein expression of senescence marker P21 and improved the relative protein expression of DNA repair protein KU70 and aging marker Lamin B1. It inhibited the activation of NF-κB, MAPKs (P38 and ERK), and mTOR pathway proteins (mTOR, 4EBP-1, and S6). Moreover, Rapalink-1 suppressed ethanol-induced mRNA expression of ICAM-1, E-selectin, MCP-1, IL-8, MMP-2, and TIMP-2. Rapalink-1 also reduced the relative protein expression of MMP-2. In summary, Rapalink-1 prevented senescence, inhibited pro-inflammatory pathway activation, and ameliorated pro-inflammatory molecule expression and MMP-2. Full article
(This article belongs to the Special Issue Alcohol-Induced Tissue and Organ Damage: Mechanisms and Therapeutic Approaches)
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22 pages, 7001 KiB  
Article
Human Alcohol-Microbiota Mice have Increased Susceptibility to Bacterial Pneumonia
by Kelly C. Cunningham, Deandra R. Smith, Daniel N. Villageliú, Christi M. Ellis, Amanda E. Ramer-Tait, Jeffrey D. Price, Todd A. Wyatt, Daren L. Knoell, Mystera M. Samuelson, Patricia E. Molina, David A. Welsh and Derrick R. Samuelson
Cells 2023, 12(18), 2267; https://doi.org/10.3390/cells12182267 - 13 Sep 2023
Cited by 1 | Viewed by 1531
Abstract
Preclinical studies have shown that chronic alcohol abuse leads to alterations in the gastrointestinal microbiota that are associated with behavior changes, physiological alterations, and immunological effects. However, such studies have been limited in their ability to evaluate the direct effects of alcohol-associated dysbiosis. [...] Read more.
Preclinical studies have shown that chronic alcohol abuse leads to alterations in the gastrointestinal microbiota that are associated with behavior changes, physiological alterations, and immunological effects. However, such studies have been limited in their ability to evaluate the direct effects of alcohol-associated dysbiosis. To address this, we developed a humanized alcohol-microbiota mouse model to systematically evaluate the immunological effects of chronic alcohol abuse mediated by intestinal dysbiosis. Germ-free mice were colonized with human fecal microbiota from individuals with high and low Alcohol Use Disorders Identification Test (AUDIT) scores and bred to produce human alcohol-associated microbiota or human control-microbiota F1 progenies. F1 offspring colonized with fecal microbiota from individuals with high AUDIT scores had increased susceptibility to Klebsiella pneumoniae and Streptococcus pneumoniae pneumonia, as determined by increased mortality rates, pulmonary bacterial burden, and post-infection lung damage. These findings highlight the importance of considering both the direct effects of alcohol and alcohol-induced dysbiosis when investigating the mechanisms behind alcohol-related disorders and treatment strategies. Full article
(This article belongs to the Special Issue Alcohol-Induced Tissue and Organ Damage: Mechanisms and Therapeutic Approaches)
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10 pages, 1667 KiB  
Article
Ethanol Exposure to Ethanol-Oxidizing HEPG2 Cells Induces Intracellular Protein Aggregation
by Paul G. Thomes, Gage Rensch, Carol A. Casey and Terrence M. Donohue, Jr.
Cells 2023, 12(7), 1013; https://doi.org/10.3390/cells12071013 - 26 Mar 2023
Cited by 1 | Viewed by 2088
Abstract
Background: Aggresomes are collections of intracellular protein aggregates. In liver cells of patients with alcoholic hepatitis, aggresomes appear histologically as cellular inclusions known as Mallory–Denk (M–D) bodies. The proteasome is a multicatalytic intracellular protease that catalyzes the degradation of both normal (native) and [...] Read more.
Background: Aggresomes are collections of intracellular protein aggregates. In liver cells of patients with alcoholic hepatitis, aggresomes appear histologically as cellular inclusions known as Mallory–Denk (M–D) bodies. The proteasome is a multicatalytic intracellular protease that catalyzes the degradation of both normal (native) and abnormal (misfolded and/or damaged) proteins. The enzyme minimizes intracellular protein aggregate formation by rapidly degrading abnormal proteins before they form aggregates. When proteasome activity is blocked, either by specific inhibitors or by intracellular oxidants (e.g., peroxynitrite, acetaldehyde), aggresome formation is enhanced. Here, we sought to verify whether inhibition of proteasome activity by ethanol exposure enhances protein aggregate formation in VL-17A cells, which are recombinant, ethanol-oxidizing HepG2 cells that express both alcohol dehydrogenase (ADH) and cytochrome P450 2E1 (CYP2E1). Methods: We exposed ethanol-non-oxidizing HepG2 cells (ADH−/CYP2E1−) or ethanol-oxidizing VL-17A (ADH+/CYP2E1+) to varying levels of ethanol for 24 h or 72 h. After these treatments, we stained cells for aggresomes (detected microscopically) and quantified their numbers and sizes. We also conducted flow cytometric analyses to confirm our microscopic findings. Additionally, aggresome content in liver cells of patients with alcohol-induced hepatitis was quantified. Results: After we exposed VL-17A cells to increasing doses of ethanol for 24 h or 72 h, 20S proteasome activity declined in response to rising ethanol concentrations. After 24 h of ethanol exposure, aggresome numbers in VL-17A cells were 1.8-fold higher than their untreated controls at all ethanol concentrations employed. After 72 h of ethanol exposure, mean aggresome numbers were 2.5-fold higher than unexposed control cells. The mean aggregate size in all ethanol-exposed VL-17A cells was significantly higher than in unexposed control cells but was unaffected by the duration of ethanol exposure. Co-exposure of cells to EtOH and rapamycin, the latter an autophagy activator, completely prevented EtOH-induced aggresome formation. In the livers of patients with alcohol-induced hepatitis (AH), the staining intensity of aggresomes was 2.2-fold higher than in the livers of patients without alcohol use disorder (AUD). Conclusions: We conclude that ethanol-induced proteasome inhibition in ethanol-metabolizing VL-17A hepatoma cells causes accumulation of protein aggregates. Notably, autophagy activation removes such aggregates. The significance of these findings is discussed. Full article
(This article belongs to the Special Issue Alcohol-Induced Tissue and Organ Damage: Mechanisms and Therapeutic Approaches)
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