Skip Navigation


Cardiovascular Research Advance Access originally published online on October 7, 2009
Cardiovascular Research 2009 84(3):337-338; doi:10.1093/cvr/cvp329
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
84/3/337    most recent
cvp329v2
cvp329v1
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Wang, Y.
Right arrow Articles by Cheng, Y.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, Y.
Right arrow Articles by Cheng, Y.
Related Collections
Right arrowRelated Article
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

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

Yves Wang1,2 and Yuanna Cheng1,*

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 . . . [Full Text of this Article]


    Funding
 

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?

Related Article

Cx43 CT domain influences infarct size and susceptibility to ventricular tachyarrhythmias in acute myocardial infarction
Karen Maass, Sharon E. Chase, Xianming Lin, and Mario Delmar
Cardiovasc Res 2009 84: 361-367. [Abstract] [Full Text] [PDF]