ArticleToxicology mechanisms and methods2016
Connexin32: a mediator of acetaminophen-induced liver injury?
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 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- The multiple mechanisms and modes of cell death after acetaminophen overdose.Exploration of digestive diseases · 2025Article
- Aedes aegypti mosquito saliva ameliorates acetaminophen-induced liver injury in mice.PloS one · 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
- Connexin hemichannel inhibition reduces acetaminophen-induced liver injury in mice.Toxicology letters · 2017Article
- Inhibition of pannexin1 channels alleviates acetaminophen-induced hepatotoxicity.Archives of toxicology · 2017Article
- The role of gap junctions in inflammatory and neoplastic disorders (Review).International journal of molecular medicine · 2017Review
- Connexin-based signaling and drug-induced hepatotoxicity.Journal of clinical and translational research · 2017Article
- Connexin32 deficiency is associated with liver injury, inflammation and oxidative stress in experimental non-alcoholic steatohepatitis.Clinical and experimental pharmacology & physiology · 2017Article
- Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology.Journal of clinical and translational research · 2017Article
- Connexins and their channels in inflammation.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Connexin32 is the building block of hepatocellular gap junctions, which control direct intercellular communication and thereby act as goalkeepers of liver homeostasis. This study was set up to investigate whether connexin32 is involved in hepatotoxicity induced by the analgesic and antipyretic drug acetaminophen. To this end, whole body connexin32 knock-out mice were overdosed with acetaminophen followed by sampling at different time points within a 24-h time frame. Evaluation was done based upon a series of clinically and mechanistically relevant read-outs, including protein adduct formation, histopathological examination, measurement of alanine aminotransferase activity, cytokine production, levels of reduced and oxidized glutathione and hepatic protein amounts of proliferating cell nuclear antigen. In essence, it was found that genetic ablation of connexin32 has no influence on several key events in acetaminophen-induced hepatotoxicity, including cell death, inflammation or oxidative stress, yet it does affect production of protein adducts as well as proliferating cell nuclear antigen steady-state protein levels. This outcome is not in line with previous studies, which are contradicting on their own, as both amplification and alleviation of this toxicological process by connexin32 have been described. This could question the suitability of the currently available models and tools to investigate the role of connexin32 in acetaminophen-triggered hepatotoxicity.
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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.