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Gap junction remodelling after myocardial infarction: is iNOS the major culprit?
Author(s) -
Boucher François
Publication year - 2008
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2008.01877_1.x
Subject(s) - culprit , citation , editorial board , library science , myocardial infarction , medicine , computer science , cardiology
Guest EditorInternational audienceThe study shows that the reduction in myocardial Cx43 content 2 weeks after cardiac infarction is less in iNOS−/− than in wild-type (WT) mice. Moreover, iNOS deficiency preserves the ratio of the phosphorylated to nonphosphorylated Cx43, improves cardiac function and increases survival. Finally, in vitro experiments demonstrate that exogenous NO production dose-dependently decreases Cx43 content in isolated cardiomyocytes