Skip Navigation



Cardiovascular Research Advance Access [Accepted Manuscript] published online on December 2, 2008

Cardiovascular Research, doi:10.1093/cvr/cvn333
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
81/3/482    most recent
cvn333v2
cvn333v1
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 Sun, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sun, Y.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

MYOCARDIAL REPAIR/REMODELING FOLLOWING INFARCTION: ROLES OF LOCAL FACTORS

Yao Sun, MD, PhD

Division of Cardiovascular Diseases Department of Medicine University of Tennessee Health Science Center Memphis, Tennessee USA

Correspondence: Yao Sun, MD, Ph.D. Division of Cardiovascular Diseases Department of Medicine University of Tennessee Health Science Center 956 Court Ave, Box 20 Memphis, TN 38163 USA Tel: (901) 448-4921 Fax: (901) 448-4921 Email: yasun{at}utmem.edu

Heart failure is a global health problem, appearing most commonly in patients with previous myocardial infarction (MI). Cardiac remodeling, particularly fibrosis seen in both the infarcted and noninfarcted myocardium are recognized to be a major determinant of the development of impaired ventricular function, leading to a poor prognosis. Elucidating cellular and molecular mechanisms responsible for the accumulation of extracellular matrix is essential for designing cardioprotective and reparative strategies that could regress fibrosisafter infarction. Multiple factors contribute to left ventricular remodeling at different stages postMI. This review will discuss the role of oxidative stress and locally produced angiotensin (Ang)II in the pathogenesis of myocardial repair/remodeling after MI.


Time for primary review: 27 Days


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
D. A. Brown and W. E. Cascio
'Leaky' ryanodine receptors and sudden cardiac death
Cardiovasc Res, October 28, 2009; (2009) cvp330v2.
[Full Text] [PDF]


Home page
DMMHome page
K. D. Boudoulas and A. K. Hatzopoulos
Cardiac repair and regeneration: the Rubik's cube of cell therapy for heart disease
Dis. Model. Mech., July 1, 2009; 2(7-8): 344 - 358.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
K. Venkatachalam, B. Venkatesan, A. J. Valente, P. C. Melby, S. Nandish, J. E. B. Reusch, R. A. Clark, and B. Chandrasekar
WISP1, a Pro-mitogenic, Pro-survival Factor, Mediates Tumor Necrosis Factor-{alpha} (TNF-{alpha})-stimulated Cardiac Fibroblast Proliferation but Inhibits TNF-{alpha}-induced Cardiomyocyte Death
J. Biol. Chem., May 22, 2009; 284(21): 14414 - 14427.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
J. Diez and G. Ertl
A translational approach to myocardial remodelling
Cardiovasc Res, February 15, 2009; 81(3): 409 - 411.
[Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.