Skip Navigation

Cardiovascular Research 2002 55(1):9-12; doi:10.1016/S0008-6363(02)00434-0
© 2002 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 Ausma, J.
Right arrow Articles by Borgers, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ausma, J.
Right arrow Articles by Borgers, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2002, European Society of Cardiology

Dedifferentiation of atrial cardiomyocytes: from in vivo to in vitro

Jannie Ausmaa,* and Marcel Borgersb

aDepartment of Physiology, Cardiovascular Research Institute Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands
bDepartment of Molecular Cell Biology, Cardiovascular Research Institute Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands

* Corresponding author. Tel.: +31-43-388-1076; fax +31-43-388-4166 jannie.ausma@fys.unimaas.nl

Received 9 April 2002; accepted 9 April 2002

The first 150 words of the full text of this article appear below.

See article by Rücker-Martin et al. [3] (pages 38–52) in this issue.


   1. Introduction
 
Atrial fibrillation (AF) is characterized by extensive electrical and structural remodeling [1,2]. The latter aspects have been associated with cardiomyocyte dedifferentiation because of the phenotypic similarities with fetal cardiomyocytes. The paper of Rücker-Martin et al. [3] in this issue describes the dedifferentiation of atrial myocytes both in vivo and in vitro and emphasizes the role of fibroblasts in the maintenance of the dedifferentiated state of the cardiomyocytes. The authors report that in biopsies from patients with AF, concomitantly suffering from valvular disease, the majority of atrial myocytes undergo changes which are reminiscent of dedifferentiation, akin to those seen in ventricular biopsies of patients with hibernating myocardium [1]. The atrial cardiomyocytes are myolytic, accumulate glycogen and myocyte bundles are separated by thick layers of fibrotic tissue. Reexpression and redistribution of structural proteins such as {alpha}-smooth muscle actin . . . [Full Text of this Article]


   2. Structural remodeling of atrial myocytes
 

   3. Are the phenotypic adaptations part of a cell survival program?
 

   4. The role of extracellular matrix and fibroblasts
 

   5. In vitro simulation of structural remodeling
 

   6. Role of stretch in initiation and maintenance of the dedifferentiated phenotype
 

   7. Unsolved issues and future perspectives
 

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


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
C. Ancey, E. Menet, P. Corbi, S. Fredj, M. Garcia, C. Rucker-Martin, J. Bescond, F. Morel, J. Wijdenes, J.-C. Lecron, et al.
Human cardiomyocyte hypertrophy induced in vitro by gp130 stimulation
Cardiovasc Res, July 1, 2003; 59(1): 78 - 85.
[Abstract] [Full Text] [PDF]