Cellular and Molecular Mechanisms of Alcohol-Induced Cellular/Organ Injury and Regeneration

A Special Issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 September 2026 | Viewed by 2322

Editor


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Guest Editor
Department of Pathology, University of Texas Medical Branch Galveston, 301 University Blvd., Galveston, TX 77550, USA
Interests: pancreas; liver; alcohol

Special Issue Information

Dear Colleagues,

This Special Issue focuses on the cellular and molecular mechanisms underlying alcohol-induced injury and regeneration in various organs. Chronic and acute alcohol exposure can trigger complex biochemical and cellular responses, leading to inflammation, oxidative stress, mitochondrial dysfunction, and tissue remodeling across multiple organ systems, including the liver, pancreas, lung, brain, and gut. This Special Issue welcomes original research and review articles that explore mechanisms of alcohol-induced cellular damage, tissue-specific responses, stem cell activation, immune modulation, and regenerative processes. Studies employing in vitro models, animal systems, and human tissues, particularly those integrating multi-omics, imaging, and molecular biology techniques, are encouraged. Contributions that shed light on potential therapeutic targets or strategies for mitigating alcohol-related pathologies and enhance tissue repair are especially welcome. By deepening our understanding of alcohol’s impact at the cellular level, this Special Issue will advance translational insights into alcohol-related diseases.

Dr. Mukund Srinivasan
Guest Editor

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Keywords

  • alcohol use disorder
  • ethanol
  • liver
  • lung
  • pancreas
  • gut
  • brain
  • cellular toxicity
  • alcohol metabolism
  • alcohol metabolites
  • oxidative stress
  • mitochondrial stress
  • ER stress

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Published Papers (1 paper)

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Research

33 pages, 10815 KB  
Article
Lipid Metabolic Changes and Mitochondrial Stress in Ethanol-Treated Alveolar Type II Epithelial Cells: Initial Events Leading to Alcoholic Chronic Lung Disease
by Mukund Srinivasan and Bhupendra S. Kaphalia
Cells 2025, 14(22), 1817; https://doi.org/10.3390/cells14221817 - 19 Nov 2025
Cited by 1 | Viewed by 1689
Abstract
Alcohol use disorder (AUD) predisposes individuals to pneumonia, acute respiratory distress syndrome, and chronic obstructive pulmonary disease, yet the mechanisms underlying alcohol-related lung disease (ARLD) remain unclear. Alveolar type II (AT2) epithelial cells play a central role in ethanol (EtOH) metabolism, surfactant production, [...] Read more.
Alcohol use disorder (AUD) predisposes individuals to pneumonia, acute respiratory distress syndrome, and chronic obstructive pulmonary disease, yet the mechanisms underlying alcohol-related lung disease (ARLD) remain unclear. Alveolar type II (AT2) epithelial cells play a central role in ethanol (EtOH) metabolism, surfactant production, alveolar repair, and pulmonary innate immunity. To examine EtOH-mediated effects, immortalized human AT2 cells were treated with 22–130 mM EtOH for 6 h (concentration-dependent) and 65 mM EtOH for 6–72 h (time-dependent). Cytotoxicity, inflammation, surfactant lipid/protein dysregulation, fatty acid ethyl ester (FAEE) formation, cellular stress responses, AMP-activated protein kinase (AMPKα) signaling, and mitochondrial function were analyzed. EtOH disrupted surfactant homeostasis by reducing dipalmitoylphosphatidylcholine and surfactant protein C (SP-C). Importantly, EtOH inactivated AMPKα, downregulated CPT1A (involved in β-oxidation of fatty acids), and upregulated lipogenic proteins ACC1 and FAS, accompanied by increased ER stress markers (GRP78, p-eIF2α, and CHOP). Expression of carboxyl ester lipase (FAEE-synthesizing enzyme) and FAEE levels increased with EtOH exposure, further exacerbating oxidative and ER stress, impairing mitochondrial energetics, ATP production, and AT2 cell function. These findings suggest that EtOH-induced FAEE formation, dysregulation of AMPKα-CPT1A signaling, and surfactant contribute to AT2 cell dysfunction and play a critical role in the pathogenesis of ARLD. Full article
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