ArticleToxicology mechanisms and methods2016
Connexin32 deficiency exacerbates carbon tetrachloride-induced hepatocellular injury and liver fibrosis in mice.
Article in Toxicology mechanisms and methods, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Effects of acute and chronic disease on cell junctions in mouse liver.EXCLI journal · 2023Article
- Expression of connexins and pannexins in diseased human liver.EXCLI journal · 2022Article
- Cholestasis Differentially Affects Liver Connexins.International journal of molecular sciences · 2020Article
- Effects of Pristine CDigestive diseases and sciences · 2020Article
- Genetic ablation of pannexin1 counteracts liver fibrosis in a chemical, but not in a surgical mouse model.Archives of toxicology · 2018Article
- TAT-Gap19 and Carbenoxolone Alleviate Liver Fibrosis in Mice.International journal of molecular sciences · 2018Article
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveLiver fibrosis results from the perpetuation of the normal wound healing response to several types of injury. Despite the wealth of knowledge regarding the involvement of intracellular and extracellular signaling pathways in liver fibrogenesis, information about the role of intercellular communication mediated by gap junctions is scarce.
methodsIn this study, liver fibrosis was chemically induced by carbon tetrachloride in mice lacking connexin32, the major liver gap junction constituent. The manifestation of liver fibrosis was evaluated based on a series of read-outs, including collagen morphometric and mRNA analysis, oxidative stress, apoptotic, proliferative and inflammatory markers.
resultsMore pronounced liver damage and enhanced collagen deposition were observed in connexin32 knockout mice compared to wild-type animals in experimentally triggered induced liver fibrosis. No differences between both groups were noticed in apoptotic signaling nor in inflammation markers. However, connexin32 deficient mice displayed decreased catalase activity and increased malondialdehyde levels.
conclusionThese findings could suggest that connexin32-based signaling mediates tissue resistance against liver damage by the modulation of the antioxidant capacity. In turn, this could point to a role for connexin32 signaling as a therapeutic target in the treatment of liver fibrosis.
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