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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Sparad:
Bibliografiska uppgifter
I publikationen:Br J Pharmacol
Huvudupphovsmän: Boengler, Kerstin, Bulic, Marko, Schreckenberg, Rolf, Schlüter, Klaus‐Dieter, Schulz, Rainer
Materialtyp: Artigo
Språk:Inglês
Publicerad: John Wiley and Sons Inc. 2017
Ämnen:
Research Papers
Länkar: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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