Cardiovascular Research Advance Access originally published online on October 7, 2009
Cardiovascular Research 2009 84(3):337-338; doi:10.1093/cvr/cvp329
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.
The tail of Cx43: its crucial protective role in acute myocardial infarction
1 Department of Molecular Cardiology, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA
2 Department of Biomedical Engineering, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA
* Corresponding author. Tel: +1 216 445 7823; fax: +1 216 445 4166, E-mail address: chengy@ccf.org
This editorial refers to Cx43 CT domain influences infarct size and susceptibility to ventricular tachyarrhythmias in acute myocardial infarction by K. Maass et al., pp. 361–367, this issue.
| The first 10% of the full text of this article appears below. |
In the heart, synchronized contractile activity is facilitated by gap junctions, intercellular channels that underlie electrical and molecular communications between cardiac myocytes. In the ventricles of the mammalian heart, gap junctions are predominately constructed of connexin43 (Cx43) subunits. In heterozygous Cx43 knockout (Cx43/KO) mice, expression of Cx43 is roughly halved and electrical conduction in the ventricles is impaired.1 Cx43/KO mice have increased susceptibility to arrhythmias after acute myocardial infarction (MI).2
Although low-resistance communication is typically desirable, a reduction of intercellular conduction during ischaemia–reperfusion episodes can be beneficial by limiting the spread of toxic metabolites that promote tissue damage.3 Decoupling the gap junctions during
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Cardiovasc Res 2009 84: 361-367.[Abstract] [Full Text] [PDF]