|
|
||||||||
Physiologisches Institut, Justus-Liebig-Universität, D-35392 Giessen, Germany
1Correspondence: Physiologisches Institut, Justus-Liebig-Universität, Aulweg 129, D-35392 Giessen, Germany. E-Mail: Klaus-Dieter.Schlueter{at}physiologie.med.uni-giessen.de
Cardiomyocytes of adult myocardium increase their cellular mass in
response to growth stimuli. They undergo hypertrophic growth but they
do not proliferate in contrast to immature cardiomyocytes. Growth
stimuli of the adult cardiomyocytes include classical growth hormones,
various neuroendocrine factors, and the increase in mechanical load.
The signal transduction of
1-adrenoceptor stimulation
has been investigated in greatest detail and may therefore be taken as
a reference for other humoral stimuli. It involves the activation of
protein kinase C (PKC) and, downstream of PKC activation, of two
separate signaling pathways, one including the mitogen-activated
protein kinase and another including PI3-kinase and p70s6k
as key steps. Activation of the first pathway leads to re-expression of
fetal genes, activation of the second pathway to a general activation
of protein synthesis, and cellular growth. In neonatal cardiomyocytes,
mechanical stretch causes growth by an activation of an autocrine
mechanism including angiotensin II and endothelin. This mechanism does
not operate, however, in adult cardiomyocytes. A mechanism of
mechanotransduction has not yet been identified on adult cardiomyocytes
but integrins may play a part. In microgravity, the scenario of
myocardial growth stimulation is altered. On the systemic level, there
are changes in hemodynamic and neuroendocrine regulation that exert
indirect effects on the myocardium. Microgravity may also exert a
direct cellular effect by the absence of a constant gravitational load
component.Schlüter, K.-D., Piper, H. M. Regulation of
growth in the adult cardiomyocytes.
Key Words: adrenoceptors mechanotransduction microgravity MAP kinase PI3-kinase
This article has been cited by other articles:
![]() |
J. R. McMullen, T. Shioi, L. Zhang, O. Tarnavski, M. C. Sherwood, A. L. Dorfman, S. Longnus, M. Pende, K. A. Martin, J. Blenis, et al. Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy Mol. Cell. Biol., July 15, 2004; 24(14): 6231 - 6240. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Stilli, A. Sgoifo, E. Macchi, M. Zaniboni, S. De Iasio, E. Cerbai, A. Mugelli, C. Lagrasta, G. Olivetti, and E. Musso Myocardial remodeling and arrhythmogenesis in moderate cardiac hypertrophy in rats Am J Physiol Heart Circ Physiol, January 1, 2001; 280(1): H142 - H150. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Schuette and M. C. LaPointe Phorbol ester stimulates cyclooxygenase-2 expression and prostanoid production in cardiac myocytes Am J Physiol Heart Circ Physiol, August 1, 2000; 279(2): H719 - H725. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. I. Rybkin, M. E. Cross, E. M. McReynolds, R. Z. Lin, and L. M. Ballou alpha 1A Adrenergic Receptor Induces Eukaryotic Initiation Factor 4E-binding Protein 1 Phosphorylation via a Ca2+-dependent Pathway Independent of Phosphatidylinositol 3-kinase/Akt J. Biol. Chem., February 25, 2000; 275(8): 5460 - 5465. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |