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Editorial
. 2014 Mar 11;63(9):935-7.
doi: 10.1016/j.jacc.2013.10.082. Epub 2014 Jan 8.

Inhibition of proto-oncogene c-Src tyrosine kinase: toward a new antiarrhythmic strategy?

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Editorial

Inhibition of proto-oncogene c-Src tyrosine kinase: toward a new antiarrhythmic strategy?

Luisa Mestroni et al. J Am Coll Cardiol. .

Abstract

Cellular-Src (c-Src) encodes a plasma membrane-associated tyrosine protein kinase, which plays a vital role in signaling pathways related to cellular development and carcinogenesis (1,2). It was the first proto-oncogene to be described and is the cellular homologue in humans of the viral oncogene of Rous sarcoma virus, the chicken tumor virus discovered by Peyton Rous in 1911 (3). More recently, c-Src has been implicated in connexin43 (Cx43) remodeling in epicardial border zone myocytes following myocardial infarction (MI) (4).

Keywords: Src; connexin43; gap junctions; myocardial infarction; sudden death.

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Figures

Figure 1
Figure 1. Scheme of c-Src Kinase Pathway Modulating Cx43
Angiotensin II (Ang II) activates and up-regulates c-Src, which in turn causes a dysregulation and degradation of connexin43 (Cx43) with impaired gap junction function. PP1 inhibits c-Src kinase and interrupts Ang II–mediated Cx43 reduction, myocyte uncoupling, and sudden arrhythmic death. ATR-1 = angiotensin II type 1 receptor; RAS = renin-angiotensin system; VF = ventricular fibrillation; VT = ventricular tachycardia; ZO = zonula-occludens. Reproduced with permission from Sovari et al. (11).

Comment on

References

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