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First published online May 26, 2006
Journal of Experimental Biology 209, 2320-2327 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02084
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Phenotypic plasticity of adult myocardium: molecular mechanisms

Bernard Swynghedauw

Inserm U.572, Hôpital Lariboisière, 41 Bd de la Chapelle, 75475, Paris Cedex 10, France


Figure 1
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Fig. 1. Working hypothesis summarizing the relationships of molecular events that drive CR. This synopsis is drawn from several recent review articles (Swynghedauw, 1999Go; Bogoyevitch, 2000Go; Akazawa and Komuro, 2003Go; Sugden, 2003Go; Knöll et al., 2003Go; Barki-Harrington and Rockman, 2003Go; Katsumi et al., 2004Go). The hypothesis is based on the sequence of events proposed elsewhere (MacLellan and Schneider, 2000Go). It includes a mechanical trigger, a cytoplasmic cascade, and then a series of phosphorylations/dephosphorylations that finally activate several transcription factors. These factors are known to act synergistically in a combinatorial fashion. It is hypothesized that (i) the foetal reprogramming depends upon transcription factors expressed during embryogenesis, and (ii) non-specific gene activation is a consequence of growth factor secretion. The scheme does not include autocrine/paracrine factors. The functions of the immediate early genes are unknown; several of them are not translated into proteins (Snoeckx et al., 1991Go).

 





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