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The gap junction modifier ZP1609 decreases cardiomyocyte hypercontracture following ischaemia/reperfusion independent from mitochondrial connexin 43
BACKGROUND AND PURPOSE: Dysregulation of gap junction‐mediated cell coupling contributes to development of arrhythmias and myocardial damage after ischaemia/reperfusion (I/R). Connexin 43 (Cx43) is present at ventricular gap junctions and also in the mitochondria of cardiomyocytes. The dipeptide (2S...
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| Pubblicato in: | Br J Pharmacol |
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| Autori principali: | , , , , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
John Wiley and Sons Inc.
2017
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| Soggetti: | |
| Accesso online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5466543/ https://ncbi.nlm.nih.gov/pubmed/28369703 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/bph.13804 |
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