ArticleNaunyn-Schmiedeberg's archives of pharmacology2013
The antiarrhythmic dipeptide ZP1609 (danegaptide) when given at reperfusion reduces myocardial infarct size in pigs.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection.Basic research in cardiology · 2018Guideline
- Rotigaptide protects the myocardium and arterial vasculature from ischaemia reperfusion injury.British journal of clinical pharmacology · 2016Trial
- Conventional Antiarrhythmics Class I-IV, Late INa Inhibitors, IKs Enhancers, RyR2 Stabilizers, Gap Junction Modulators, Atrial-Selective Antiarrhythmics, and Stable Gastric Pentadecapeptide BPC 157 as Useful Cytoprotective Therapy in Arrhythmias.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Deep learning segmentation model for quantification of infarct size in pigs with myocardial ischemia/reperfusion.Basic research in cardiology · 2024Article
- Connexin hemichannels as candidate targets for cardioprotective and anti-arrhythmic treatments.The Journal of clinical investigation · 2023Review
- 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
- Mechanisms of Connexin Regulating Peptides.International journal of molecular sciences · 2021Review
- Peptidic Connexin43 Therapeutics in Cardiac Reparative Medicine.Journal of cardiovascular development and disease · 2021Review
- Rotigaptide Infusion for the First 7 Days After Myocardial Infarction-Reperfusion Reduced Late Complexity of Myocardial Architecture of the Healing Border-Zone and Arrhythmia Inducibility.Journal of the American Heart Association · 2021Article
- GJA1-20k attenuates Ang II-induced pathological cardiac hypertrophy by regulating gap junction formation and mitochondrial function.Acta pharmacologica Sinica · 2021Article
- Danegaptide Prevents TGFβ1-Induced Damage in Human Proximal Tubule Epithelial Cells of the Kidney.International journal of molecular sciences · 2021Article
- Canonical and Non-Canonical Roles of Connexin43 in Cardioprotection.Biomolecules · 2020Review
- Danegaptide Enhances Astrocyte Gap Junctional Coupling and Reduces Ischemic Reperfusion Brain Injury in Mice.Biomolecules · 2020Article
- Larger infarct size but equal protection by ischemic conditioning in septum and anterior free wall of pigs with LAD occlusion.Physiological reports · 2019Article
- A humanAPL bioengineering · 2019Article
- Therapeutic strategies targeting connexins.Nature reviews. Drug discovery · 2018Review
- Connexins and Disease.Cold Spring Harbor perspectives in biology · 2018Review
- Connexins: Synthesis, Post-Translational Modifications, and Trafficking in Health and Disease.International journal of molecular sciences · 2018Review
- Acute connexin43 temporal and spatial expression in response to ischemic stroke.Journal of cell communication and signaling · 2018Article
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Connexin 43 is located in the cardiomyocyte sarcolemma and in the mitochondrial membrane. Sarcolemmal connexin 43 contributes to the spread of myocardial ischemia/reperfusion injury, whereas mitochondrial connexin 43 contributes to cardioprotection. We have now investigated the antiarrhythmic dipeptide ZP1609 (danegaptide), which is an analog of the connexin 43 targeting antiarrhythmic peptide rotigaptide (ZP123), in an established and clinically relevant experimental model of ischemia/reperfusion in pigs. Pigs were subjected to 60 min coronary occlusion and 3 h reperfusion. ZP1609 (n = 10) was given 10 min prior to reperfusion (75 μg/kg b.w. bolus i.v. + 57 μg/kg/min i.v. infusion for 3 h). Immediate full reperfusion (IFR, n = 9) served as control. Ischemic postconditioning (PoCo, n = 9; 1 min LAD reocclusion after 1 min reperfusion; four repetitions) was used as a positive control of cardioprotection. Infarct size (TTC) was determined as the end point of cardioprotection. Systemic hemodynamics and regional myocardial blood flow during ischemia were not different between groups. PoCo and ZP1609 reduced infarct size vs. IFR (IFR, 46 ± 4 % of area at risk; mean ± SEM; PoCo, 31 ± 4 %; ZP1609, 25 ± 5 %; both p < 0.05 vs. IFR; ANOVA). There were only few arrhythmias during reperfusion such that no antiarrhythmic action of ZP1609 was observed. ZP1609 when given before reperfusion reduces infarct size to a similar extent as ischemic postconditioning. Further studies are necessary to define the mechanism/action of ZP1609 on connexin 43 in cardiomyocytes.
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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.