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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Udgivet i:Br J Pharmacol
Main Authors: Boengler, Kerstin, Bulic, Marko, Schreckenberg, Rolf, Schlüter, Klaus‐Dieter, Schulz, Rainer
Format: Artigo
Sprog:Inglês
Udgivet: John Wiley and Sons Inc. 2017
Fag:
Research Papers
Online adgang: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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