ReviewBritish journal of pharmacology2011
Pharmacological modulation of connexin-formed channels in cardiac pathophysiology.
Review in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 92 citations in OpenAlex.
- Review
- A multiscale computational model of cardiac electrophysiology for drug-induced pro-arrhythmic risk stratification.Biomedical engineering letters · 2026Article
- Capacitance-Driven Modulation of Cardiac Impulse Conduction by an Intramembrane Molecular Photoswitch.International journal of molecular sciences · 2025Article
- Overexpression of Cx43: Is It an Effective Approach for the Treatment of Cardiovascular Diseases?Biomolecules · 2025Review
- Mapping the Anti-Cancer Activity of α-Connexin Carboxyl-Terminal (aCT1) Peptide in Resistant HER2+ Breast Cancer.Cancers · 2024Article
- Mechanism of connexin channel inhibition by mefloquine and 2-aminoethoxydiphenyl borate.PloS one · 2024Article
- Evaluation of Cx43 Gap Junction Inhibitors Using a Quantitative Structure-Activity Relationship Model.Biomedicines · 2023Article
- Electrophysiological Changes of Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes during Acute Hypoxia and Reoxygenation.Stem cells international · 2022Article
- Mechanisms of Connexin Regulating Peptides.International journal of molecular sciences · 2021Review
- Review
- Danegaptide Prevents TGFβ1-Induced Damage in Human Proximal Tubule Epithelial Cells of the Kidney.International journal of molecular sciences · 2021Article
- Attenuating loss of cardiac conduction during no-flow ischemia through changes in perfusate sodium and calcium.American journal of physiology. Heart and circulatory physiology · 2020Article
- Cardiac β-adrenergic receptor activation mediates distinct and cell type-dependent changes in the expression and distribution of connexin 43.Journal of cellular and molecular medicine · 2020Article
- Connexin 43 Mutations Lead to Increased Hemichannel Functionality in Skin Disease.International journal of molecular sciences · 2019Review
- A humanAPL bioengineering · 2019Article
- Overview of the Components of Cardiac Metabolism.Drug metabolism and disposition: the biological fate of chemicals · 2019Review
- Antiarrhythmic effect of sevoflurane as an additive to HTK solution on reperfusion arrhythmias induced by hypothermia and ischaemia is associated with the phosphorylation of connexin 43 at serine 368.BMC anesthesiology · 2019Article
- Translational Models of Arrhythmia Mechanisms and Susceptibility: Success and Challenges of Modeling Human Disease.Frontiers in cardiovascular medicine · 2019Review
- Article
- Inhibition of Connexin Hemichannels by New Amphiphilic Aminoglycosides without Antibiotic Activity.ACS medicinal chemistry letters · 2018Article
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 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coordinated electrical activity in the heart is supported by gap junction channels located at the intercalated discs of cardiomyocytes. Impaired gap junctional communication between neighbouring cardiomyocytes contributes to the development of re-entry arrhythmias after myocardial ischaemia. Current antiarrhythmic therapy is hampered by a lack of efficiency and side effects, creating the need for a new generation of drugs. In this review, we focus on compounds that increase gap junctional communication, thereby increasing the conduction velocity and decreasing the risk of arrhythmias. Some of these compounds also inhibit connexin 43 (Cx43) hemichannels, thereby limiting adenosine triphosphate loss and volume overload following ischaemia/reperfusion, thus potentially increasing the survival of cardiomyocytes. The compounds discussed in this review are: (i) antiarrythmic peptide (AAP), AAP10, ZP123; (ii) GAP-134; (iii) RXP-E; and (vi) the Cx mimetic peptides Gap 26 and Gap 27. None of these compounds have effects on Na(+) , Ca(2+) and K(+) channels, and therefore have no proarrhythmic activity associated with currently available antiarrhythmic drugs. GAP-134, RXP-E, Gap 26 and Gap 27 are pharmalogical agents with a favorable clinical safety profile, as already confirmed in phase I clinical trials for GAP-134. These agents show an excellent promise for treatment of arrhythmias in patients with ischaemic cardiomyopathy.
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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.