ArticleAlcoholism, clinical and experimental research2017
Myeloid-MyD88 Contributes to Ethanol-Induced Liver Injury in Mice Linking Hepatocellular Death to Inflammation.
Article in Alcoholism, clinical and experimental research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Gut-liver axis molecular mechanisms in alcohol-associated liver disease.Alcohol (Fayetteville, N.Y.) · 2026Review
- Toll/IL-1 receptor domain-containing adaptor protein plays a crucial role in macrophage-mediated hepatic stellate cell activation in alcoholic liver disease.Frontiers in cell and developmental biology · 2026Article
- MyD88 in hepatic stellate cells promotes the development of alcoholic fatty liver via the AKT pathway.Journal of molecular medicine (Berlin, Germany) · 2022Article
- The Role of Gut Bacteria and Fungi in Alcohol-Associated Liver Disease.Frontiers in medicine · 2022Review
- Cell Death in Liver Diseases: A Review.International journal of molecular sciences · 2020Review
- Inhibition of IRAK4 kinase activity improves ethanol-induced liver injury in mice.Journal of hepatology · 2020Article
- Restricted immunological and cellular pathways are shared by murine models of chronic alcohol consumption.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundToll-like receptor 4 (TLR4) is critical for ethanol (EtOH)-induced liver injury. TLR4 signaling is mediated by 2 proximal adaptor molecules: myeloid differentiation primary response protein (MyD88) and TLR-domain-containing adaptor-inducing interferon-β (TRIF). Studies utilizing global knockouts of MyD88 and TRIF identified a predominant role for TRIF signaling in the progression of EtOH-induced liver injury. In contrast, IL-1 receptor, which signals solely via the MyD88 pathway, is also known to mediate EtOH-induced liver injury. We postulated that a cell-specific role for MyD88 in myeloid cells might explain these apparently discrepant roles of MyD88. Here we made use of myeloid-specific MyD88-deficient (MyD88
methodsMyD88
resultsLittermate control, but not MyD88
conclusionsCollectively, these data demonstrate a cell-specific role for MyD88 in the development of chronic EtOH-induced liver injury. While MyD88
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.