ArticleToxicology letters2017
Connexin hemichannel inhibition reduces acetaminophen-induced liver injury in mice.
Article in Toxicology letters, 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, 37 citations in OpenAlex.
- Hepsin as a potential therapeutic target for alleviating acetaminophen-induced hepatotoxicity via gap-junction regulation and oxidative stress modulation.Cell biology and toxicology · 2024Article
- Understanding the Role of Connexins in Hepatocellular Carcinoma: Molecular and Prognostic Implications.Cancers · 2024Review
- Assessment of Connexin43 Hemichannel Functionality Based on Cytosolic Uptake of Yo-Pro1.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Connexin 43 and Pannexin 1 hemichannels as endogenous regulators of innate immunity in sepsis.Frontiers in immunology · 2024Review
- Nanobody-based pannexin1 channel inhibitors reduce inflammation in acute liver injury.Journal of nanobiotechnology · 2023Article
- MgIG Attenuates Oxaliplatin-induced Hepatotoxicity through Suppression of Connexin 43 in Hepatic Stellate Cells.Journal of clinical and translational hepatology · 2023Article
- Review
- Connexin 43: A Target for the Treatment of Inflammation in Secondary Complications of the Kidney and Eye in Diabetes.International journal of molecular sciences · 2022Review
- Connexin-Based Channel Activity Is Not Specifically Altered by Hepatocarcinogenic Chemicals.International journal of molecular sciences · 2021Article
- Mechanisms of Connexin Regulating Peptides.International journal of molecular sciences · 2021Review
- The Relationship between theIranian journal of medical sciences · 2021Article
- Primary Osteocyte Supernatants Metabolomic Profiling of Two Transgenic Mice With Connexin43 Dominant Negative Mutants.Frontiers in endocrinology · 2021Article
- Propagation of Pericentral Necrosis During Acetaminophen-Induced Liver Injury: Evidence for Early Interhepatocyte Communication and Information Exchange.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Contribution of Connexin Hemichannels to the Decreases in Cell Viability Induced by Linoleic Acid in the Human Lens Epithelial Cells (HLE-B3).Frontiers in physiology · 2019Article
- Structural determinants of COCommunications biology · 2019Article
- The Role of Connexin-43 in the Inflammatory Process: A New Potential Therapy to Influence Keratitis.Journal of ophthalmology · 2019Review
- Transforming growth factor-β1 up-regulates connexin43 expression in osteocytes via canonical Smad-dependent signaling pathway.Bioscience reports · 2018Article
- The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response.International journal of molecular sciences · 2018Review
- 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
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Historically, connexin hemichannels have been considered as structural precursors of gap junctions. However, accumulating evidence points to independent roles for connexin hemichannels in cellular signaling by connecting the intracellular compartment with the extracellular environment. Unlike gap junctions, connexin hemichannels seem to be mainly activated in pathological processes. The present study was set up to test the potential involvement of hemichannels composed of connexin32 and connexin43 in acute hepatotoxicity induced by acetaminophen. Prior to this, in vitro testing was performed to confirm the specificity and efficacy of TAT-Gap24 and TAT-Gap19 in blocking connexin32 and connexin43 hemichannels, respectively. Subsequently, mice were overdosed with acetaminophen followed by treatment with TAT-Gap24 or TAT-Gap19 or a combination of both after 1.5h. Sampling was performed 3, 6, 24 and 48h following acetaminophen administration. Evaluation of the effects of connexin hemichannel inhibition was based on a series of clinically relevant read-outs, measurement of inflammatory cytokines and oxidative stress. Subsequent treatment of acetaminophen-overdosed mice with TAT-Gap19 only marginally affected liver injury. In contrast, a significant reduction in serum alanine aminotransferase activity was found upon administration of TAT-Gap24 to intoxicated animals. Furthermore, co-treatment of acetaminophen-overdosed mice with both peptides revealed an additive effect as even lower serum alanine aminotransferase activity was observed. Blocking of connexin32 or connexin43 hemichannels individually was found to decrease serum quantities of pro-inflammatory cytokines, while no effects were observed on the occurrence of hepatic oxidative stress. This study shows for the first time a role for connexin hemichannels in acetaminophen-induced acute liver failure.
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