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Cardiovascular Research 2001 51(2):191-193; doi:10.1016/S0008-6363(01)00352-2
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Cellular models of hibernating myocardium: implications for future research

G.Chad Hughes*

Division of Cardiovascular and Thoracic Surgery, Duke University Medical Center, Box 31224, Durham, NC 27710, USA

chadh@duke.edu

* Tel.: +1-919-684-3235; fax: +1-919-681-7524

Received 28 May 2001; accepted 29 May 2001

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

See article by Dispersyn et al. [1] (pages 230–240) in this issue.


   1 Introduction
 
In the current issue of Cardiovascular Research, Dispersyn and colleagues [1] describe a novel in vitro model of cardiomyocyte de-differentiation similar to that seen in hibernating myocardium. By co-culturing adult rabbit cardiomyocytes with cardiac fibroblasts, ultrastructural changes including sarcomere depletion and disalignment, appearance of aberrantly shaped mini-mitochondria, and progressive dispersion of nuclear heterochromatin were seen within the cardiomyocytes beginning several days after their establishment of cell–cell apposition with fibroblasts. These ultrastructural findings are nearly identical to those seen in both large animals [2] and humans [3] with hibernating myocardium with the one exception being that the cultured cells did not demonstrate a significant increase in glycogen content within the regions of sarcomere loss, a change typically considered among the hallmarks of hibernating myocardium [4]. In addition to the ultrastructural alterations, Dispersyn and colleagues also demonstrated changes . . . [Full Text of this Article]


   2 Development of the hibernating phenotype
 

   3 Reversal of the hibernating phenotype
 

   4 Summary
 

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