| http://purl.uniprot.org/citations/27222313 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27222313 | http://www.w3.org/2000/01/rdf-schema#comment | "Rac1 is a small GTPase and plays key roles in multiple cellular processes including the production of reactive oxygen species (ROS). However, whether Rac1 activation during myocardial ischaemia and reperfusion (I/R) contributes to arrhythmogenesis is not fully understood. We aimed to study the effects of Rac1 inhibition on store overload-induced Ca(2+) release (SOICR) and ventricular arrhythmia during myocardial I/R. Adult Rac1(f/f) and cardiac-specific Rac1 knockdown (Rac1(ckd) ) mice were subjected to myocardial I/R and their electrocardiograms (ECGs) were monitored for ventricular arrhythmia. Myocardial Rac1 activity was increased and ventricular arrhythmia was induced during I/R in Rac1(f/f) mice. Remarkably, I/R-induced ventricular arrhythmia was significantly decreased in Rac1(ckd) compared to Rac1(f/f) mice. Furthermore, treatment with Rac1 inhibitor NSC23766 decreased I/R-induced ventricular arrhythmia. Ca(2+) imaging analysis showed that in response to a 6 mM external Ca(2+) concentration challenge, SOICR was induced with characteristic spontaneous intracellular Ca(2+) waves in Rac1(f/f) cardiomyocytes. Notably, SOICR was diminished by pharmacological and genetic inhibition of Rac1 in adult cardiomyocytes. Moreover, I/R-induced ROS production and ryanodine receptor 2 (RyR2) oxidation were significantly inhibited in the myocardium of Rac1(ckd) mice. We conclude that Rac1 activation induces ventricular arrhythmia during myocardial I/R. Inhibition of Rac1 suppresses SOICR and protects against ventricular arrhythmia. Blockade of Rac1 activation may represent a new paradigm for the treatment of cardiac arrhythmia in ischaemic heart disease."xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.org/dc/terms/identifier | "doi:10.1111/jcmm.12840"xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/author | "Feng Q."xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/author | "Lu X."xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/author | "Wu Y."xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/author | "Wang G."xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/author | "Zhang L."xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/author | "Gui L."xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/author | "Sims S.M."xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/name | "J Cell Mol Med"xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/pages | "1513-1522"xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/title | "Inhibition of Rac1 reduces store overload-induced calcium release and protects against ventricular arrhythmia."xsd:string |
| http://purl.uniprot.org/citations/27222313 | http://purl.uniprot.org/core/volume | "20"xsd:string |
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