ReviewThe Journal of membrane biology2007
Possible involvement of different connexin43 domains in plasma membrane permeabilization induced by ischemia-reperfusion.
Review in The Journal of membrane biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Unravelling Contributions of Astrocytic Connexin 43 to the Functional Activity of Brain Neuron-Glial Networks under Hypoxic State In Vitro.Membranes · 2022Article
- Oxidative Stress and the Neurovascular Unit.Life (Basel, Switzerland) · 2021Review
- Peptidic Connexin43 Therapeutics in Cardiac Reparative Medicine.Journal of cardiovascular development and disease · 2021Review
- Cardiac Connexin-43 Hemichannels and Pannexin1 Channels: Provocative Antiarrhythmic Targets.International journal of molecular sciences · 2020Review
- Gap19, a Cx43 Hemichannel Inhibitor, Acts as a Gating Modifier That Decreases Main State Opening While Increasing Substate Gating.International journal of molecular sciences · 2020Article
- CU06-1004 (endothelial dysfunction blocker) ameliorates astrocyte end-feet swelling by stabilizing endothelial cell junctions in cerebral ischemia/reperfusion injury.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Mitochondrial connexin 43 in sex-dependent myocardial responses and estrogen-mediated cardiac protection following acute ischemia/reperfusion injury.Basic research in cardiology · 2019Article
- Interaction of α Carboxyl Terminus 1 Peptide With the Connexin 43 Carboxyl Terminus Preserves Left Ventricular Function After Ischemia-Reperfusion Injury.Journal of the American Heart Association · 2019Article
- Electrically conductive nanomaterials for cardiac tissue engineering.Advanced drug delivery reviews · 2019Review
- The SH3-binding domain of Cx43 participates in loop/tail interactions critical for Cx43-hemichannel activity.Cellular and molecular life sciences : CMLS · 2018Article
- Mechanisms of ATP Release by Inflammatory Cells.International journal of molecular sciences · 2018Review
- Roles of astrocytic connexin-43, hemichannels, and gap junctions in oxygen-glucose deprivation/reperfusion injury induced neuroinflammation and the possible regulatory mechanisms of salvianolic acid B and carbenoxolone.Journal of neuroinflammation · 2018Article
- Acute connexin43 temporal and spatial expression in response to ischemic stroke.Journal of cell communication and signaling · 2018Article
- Cataract-associated connexin 46 mutation alters its interaction with calmodulin and function of hemichannels.The Journal of biological chemistry · 2018Article
- A Cell-Based Assay to Assess Hemichannel Function.The Yale journal of biology and medicine · 2017Review
- Gap junctions and hemichannels: communicating cell death in neurodevelopment and disease.BMC cell biology · 2017Review
- Role of Akt and Ca2+ on cell permeabilization via connexin43 hemichannels induced by metabolic inhibition.Biochimica et biophysica acta · 2015Article
- Connexin: a potential novel target for protecting the central nervous system?Neural regeneration research · 2015Review
- Functional analysis and regulation of purified connexin hemichannels.Frontiers in physiology · 2014Review
- Possible role of hemichannels in cancer.Frontiers in physiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
In vitro and in vivo studies support the involvement of connexin 43-based cell-cell channels and hemichannels in cell death propagation induced by ischemia-reperfusion. In this context, open connexin hemichannels in the plasma membrane have been proposed to act as accelerators of cell death. Progress on the mechanisms underlying the cell permeabilization induced by ischemia-reperfusion reveals the involvement of several factors leading to an augmented open probability and increased number of hemichannels on the cell surface. While open probability can be increased by a reduction in extracellular concentration of divalent cations and changes in covalent modifications of connexin 43 (oxidation and phosphorylation), increase in number of hemichannels requires an elevation of the intracellular free Ca(2+) concentration. Reversal of connexin 43 redox changes and membrane permeabilization can be induced by intracellular, but not extracellular, reducing agents, suggesting a cytoplasmic localization of the redox sensor(s). In agreement, hemichannels formed by connexin 45, which lacks cytoplasmic cysteines, or by connexin 43 with its C-terminal domain truncated to remove its cysteines are insensitive to reducing agents. Although further studies are required for a precise localization of the redox sensor of connexin 43 hemichannels, modulation of the redox potential is proposed as a target for the design of pharmacological tools to reduce cell death induced by ischemia-reperfusion in connexin 43-expressing cells.
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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.