ReviewCell and tissue research2025
Involvement of connexin 43 in myocardial ischemia-reperfusion injury.
Review in Cell and tissue research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- From channels to communication networks: a perspective on connexins, pannexins and innexins.Cell and tissue research · 2026Article
- From Ischemic Injury to Arrhythmogenic Substrate: Molecular and Histopathological Insights into Post-Infarction Sudden Cardiac Death.Life (Basel, Switzerland) · 2026Review
- Inhibition of Pyk2 prevents Cx43 remodeling and cardiomyocyte injury during hypoxic and adrenergic stress.Journal of molecular and cellular cardiology · 2026Article
- Effect of ischemic preconditioning on the expression of Cx43 protein in intestinal ischemia-reperfusion injury in SD rats.Frontiers in physiology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Connexin 43 (Cx43) is the principal connexin isoform expressed in the ventricular myocardium, where it is critically involved in the pathophysiology of cardiac ischemia-reperfusion injury. Its functions in this pathological condition span at least three different fronts. First, Cx43-mediated gap junctional channels contribute to the spread of cellular damage during reperfusion, allowing the transfer of sodium ions between injured and surviving cardiomyocytes. Further, under ischemic conditions, unapposed Cx43 hemichannels exacerbate injury by promoting calcium overload, metabolite losses, and membrane potential instability. Additionally, recent evidence suggest that mitochondrial Cx43 influences oxidative stress by modulating reactive oxygen species generation through the regulation of reverse electron transfer (RET) at the mitochondrial electron transport chain. These detrimental roles of Cx43 in acute myocardial ischemia-reperfusion injury, together with its previously described involvement in ischemic preconditioning, emphasize the dual functionality and importance of Cx43 in the context of acute myocardial infarction. The scope of this review is to summarize the current knowledge on the different mechanisms by which Cx43 promotes cell damage during myocardial infarction, with special emphasis on the regulation of RET.
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.