ArticleScientific reports2017
Inhibition of connexin hemichannels alleviates non-alcoholic steatohepatitis in mice.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Hepatocyte nuclear factor 1 in renal lipid metabolism: molecular mechanisms and therapeutic potentials.Cell biology and toxicology · 2025Review
- Purinergic signaling in liver disease: calcium signaling and induction of inflammation.Purinergic signalling · 2025Review
- The p-STAT3/ANXA2 axis promotes caspase-1-mediated hepatocyte pyroptosis in non-alcoholic steatohepatitis.Journal of translational medicine · 2022Article
- Transcriptional control by HNF-1: Emerging evidence showing its role in lipid metabolism and lipid metabolism disorders.Genes & diseases · 2022Review
- Review
- Expression and Functionality of Connexin-Based Channels in Human Liver Cancer Cell Lines.International journal of molecular sciences · 2021Article
- Connexin-Based Channel Activity Is Not Specifically Altered by Hepatocarcinogenic Chemicals.International journal of molecular sciences · 2021Article
- The role of connexin proteins and their channels in radiation-induced atherosclerosis.Cellular and molecular life sciences : CMLS · 2021Review
- Mechanisms Underlying Connexin Hemichannel Activation in Disease.International journal of molecular sciences · 2021Review
- Clodronate, an inhibitor of the vesicular nucleotide transporter, ameliorates steatohepatitis and acute liver injury.Scientific reports · 2021Article
- Intercellular Transmission of Hepatic ER Stress in Obesity Disrupts Systemic Metabolism.Cell metabolism · 2021Article
- Purinergic Signaling in Liver Pathophysiology.Frontiers in endocrinology · 2021Review
- Dietary inclusion of Antarctic krill meal during the finishing feed period improves health and fillet quality of Atlantic salmon (The British journal of nutrition · 2020Article
- Connexin43 Hemichannel Targeting With TAT-Gap19 Alleviates Radiation-Induced Endothelial Cell Damage.Frontiers in pharmacology · 2020Article
- Genetic ablation of pannexin1 counteracts liver fibrosis in a chemical, but not in a surgical mouse model.Archives of toxicology · 2018Article
- Hepatic connexin 32 associates with nonalcoholic fatty liver disease severity.Hepatology communications · 2018Article
- The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response.International journal of molecular sciences · 2018Review
- Angiotensin II-Induced Mesangial Cell Damaged Is Preceded by Cell Membrane Permeabilization Due to Upregulation of Non-Selective Channels.International journal of molecular sciences · 2018Article
- TAT-Gap19 and Carbenoxolone Alleviate Liver Fibrosis in Mice.International journal of molecular sciences · 2018Article
- Acute connexin43 temporal and spatial expression in response to ischemic stroke.Journal of cell communication and signaling · 2018Article
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While gap junctions mediate intercellular communication and support liver homeostasis, connexin hemichannels are preferentially opened by pathological stimuli, including inflammation and oxidative stress. The latter are essential features of non-alcoholic steatohepatitis. In this study, it was investigated whether connexin32 and connexin43 hemichannels play a role in non-alcoholic steatohepatitis. Mice were fed a choline-deficient high-fat diet or normal diet for 8 weeks. Thereafter, TAT-Gap24 or TAT-Gap19, specific inhibitors of hemichannels composed of connexin32 and connexin43, respectively, were administered for 2 weeks. Subsequently, histopathological examination was carried out and various indicators of inflammation, liver damage and oxidative stress were tested. In addition, whole transcriptome microarray analysis of liver tissue was performed. Channel specificity of TAT-Gap24 and TAT-Gap19 was examined in vitro by fluorescence recovery after photobleaching analysis and measurement of extracellular release of adenosine triphosphate. TAT-Gap24 and TAT-Gap19 were shown to be hemichannel-specific in cultured primary hepatocytes. Diet-fed animals treated with TAT-Gap24 or TAT-Gap19 displayed decreased amounts of liver lipids and inflammatory markers, and augmented levels of superoxide dismutase, which was supported by the microarray results. These findings show the involvement of connexin32 and connexin43 hemichannels in non-alcoholic steatohepatitis and, simultaneously, suggest a role as potential drug targets in non-alcoholic steatohepatitis.
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