© 2002 European Society of Cardiology
Effects of the calcineurin dependent signaling pathway inhibition by cyclosporin A on early and late cardiac remodeling following myocardial infarction
a Department of Internal Medicine, College of Medicine, Chungbuk National University # 62 Gaeshin-dong, Hungduk-gu, Cheongju 361-711, South Korea
b Medical Research Institute, College of Medicine, Chungbuk National University Cheongju, South Korea
c Department of Internal Medicine, College of Medicine, Hallym University Chuncheon, South Korea
d Department of Neurosurgery, College of Medicine, Chungbuk National University Cheongju, South Korea
* Corresponding author. Tel.: +82-43-269-6356; fax: +82-43-273-3252. E-mail address: mccho{at}med.chungbuk.ac.kr
 |
Abstract |
|---|
Background: The calcineurin-mediated signaling pathway has been implicated as one of the crucial pathways in cardiac hypertrophy. However, the role of calcineurin pathway on cardiac remodeling after myocardial infarction (MI) has not been well defined.
Methods: Infarcted rats (n=45) were randomized into calcineurin inhibitor, cyclosporin A (CsA) or vehicle groups, 3 days after MI and treated for 2 weeks (early post-MI cardiac remodeling stage), or randomized 17 days after MI and treated for 2 weeks (late remodeling stage).
Results: Calcineurin pathway inhibition during the early cardiac remodeling stage attenuated the myocardial hypertrophy after MI (P<0.05). However, left ventricular dimensions were further increased and fractional shortening deteriorated with calcineurin inhibition during this stage (P<0.05, each). During late remodeling stage, CsA treatment did not affect myocardial hypertrophy and cardiac dilation following MI.
Conclusion: Our results strongly support the hypothesis that calcineurin pathway mediates compensatory myocardial hypertrophy during the early remodeling stage after MI. However, the calcineurin pathway does not seem to affect the late remodeling after MI.
Key Words: Heart failure • Hypertrophy • Infarction • Remodeling • Calcineurin
Received December 11, 2001; Revised March 18, 2002; Accepted May 21, 2002
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J.-Y. Hahn, H.-J. Cho, J.-W. Bae, H.-S. Yuk, K.-i. Kim, K.-W. Park, B.-K. Koo, I.-H. Chae, C.-S. Shin, B.-H. Oh, et al. beta-Catenin Overexpression Reduces Myocardial Infarct Size through Differential Effects on Cardiomyocytes and Cardiac Fibroblasts J. Biol. Chem., October 13, 2006; 281(41): 30979 - 30989. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Piao, T.-J. Youn, J.-S. Kwon, Y.-H. Kim, J.-W. Bae, Bora-Sohn, D.-W. Kim, M.-C. Cho, M.-M. Lee, and Y.-B. Park Effects of bone marrow derived mesenchymal stem cells transplantation in acutely infarcting myocardium Eur J Heart Fail, August 1, 2005; 7(5): 730 - 738. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. van Rooij, P. A. Doevendans, H. J.G.M. Crijns, S. Heeneman, D. J. Lips, M. van Bilsen, R. S. Williams, E. N. Olson, R. Bassel-Duby, B. A. Rothermel, et al. MCIP1 Overexpression Suppresses Left Ventricular Remodeling and Sustains Cardiac Function After Myocardial Infarction Circ. Res., February 20, 2004; 94 (3): e18 - e26. [Abstract] [Full Text] [PDF]
|
|