ArticleBiomolecules2016
Moderate (2%, v/v) Ethanol Feeding Alters Hepatic Wound Healing after Acute Carbon Tetrachloride Exposure in Mice.
Article in Biomolecules, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Evaluation of Umbelliferone Neuroprotective Effects Against Acrylamide-Induced Oxidative Stress, In Vivo and In Silico Study.Journal of molecular neuroscience : MN · 2026Article
- Hyaluronan synthesis inhibition normalizes ethanol-enhanced hepatic stellate cell activation.Alcohol, clinical & experimental research · 2023Article
- Significance of CCNs in liver regeneration.Journal of cell communication and signaling · 2023Review
- Liver regeneration and ethanol detoxification: A new link in YAP regulation of ALDH1A1 during alcohol-related hepatocyte damage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- XIAP Knockdown in Alcohol-Associated Liver Disease Models Exhibits DivergentFrontiers in physiology · 2021Article
- Hepatocyte nuclear factor 4α negatively regulates connective tissue growth factor during liver regeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Role of A-Kinase Anchoring Protein Phosphorylation in Alcohol-Induced Liver Injury and Hepatic Stellate Cell Activation.The American journal of pathology · 2018Article
- Increased YAP Activation Is Associated With Hepatic Cyst Epithelial Cell Proliferation in ARPKD/CHF.Gene expression · 2017Article
- C57BL/6 Substrains Exhibit Different Responses to Acute Carbon Tetrachloride Exposure: Implications for Work Involving Transgenic Mice.Gene expression · 2017Article
- Multi-Organ Alcohol-Related Damage: Mechanisms and Treatment.Biomolecules · 2016Article
- Inhibition of Mast Cell Degranulation With Cromolyn Sodium Exhibits Organ-Specific Effects in Polycystic Kidney (PCK) Rats.International journal of toxicologyArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Wound healing consists of three overlapping phases: inflammation, proliferation, and matrix synthesis and remodeling. Prolonged alcohol abuse can cause liver fibrosis due to deregulated matrix remodeling. Previous studies demonstrated that moderate ethanol feeding enhances liver fibrogenic markers and frank fibrosis independent of differences in CCl₄-induced liver injury. Our objective was to determine whether or not other phases of the hepatic wound healing response were affected by moderate ethanol after CCl₄ exposure. Mice were fed moderate ethanol (2% v/v) for two days and then were exposed to CCl₄ and euthanized 24-96 h later. Liver injury was not different between pair- and ethanol-fed mice; however, removal of necrotic tissue was delayed after CCl₄-induced liver injury in ethanol-fed mice. Inflammation, measured by TNFα mRNA and protein and hepatic Ly6c transcript accumulation, was reduced and associated with enhanced hepatocyte apoptosis after ethanol feeding. Hepatocytes entered the cell cycle equivalently in pair- and ethanol-fed mice after CCl₄ exposure, but hepatocyte proliferation was prolonged in livers from ethanol-fed mice. CCl₄-induced hepatic stellate cell activation was increased and matrix remodeling was prolonged in ethanol-fed mice compared to controls. Taken together, moderate ethanol affected each phase of the wound healing response to CCl₄. These data highlight previously unknown effects of moderate ethanol exposure on hepatic wound healing after acute hepatotoxicant exposure.
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Registered trials
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