Using systems biology approaches to understand cardiac inflammation and extracellular matrix remodeling in the setting of myocardial infarction-Reference-Cited by-同舟云学术

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Using systems biology approaches to understand cardiac inflammation and extracellular matrix remodeling in the setting of myocardial infarction

Published:2013-11-08 Issue:1 Volume:6 Page:77-91
ISSN:1939-5094
Container-title:Wiley Interdisciplinary Reviews: Systems Biology and Medicine
language:en
Short-container-title:WIREs Syst Biol Med

Author:

Ghasemi Omid¹²,Ma Yonggang²³,Lindsey Merry L.²³⁴,Jin Yu-Fang¹²

Affiliation:

1. Department of Electrical and Computer Engineering; The University of Texas at San Antonio; San Antonio TX USA

2. San Antonio Cardiovascular Proteomics Center; San Antonio TX USA

3. Mississippi Center for Heart Research, Department of Physiology and Biophysics; University of Mississippi Medical Center; Jackson MS USA

4. Research Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center; Jackson MS USA

Funder

National Institutes of Health

Biomedical Laboratory Research and Development Service of the Veterans Affairs Office of Research and Development Award

Publisher

Wiley

Subject

Biochemistry, Genetics and Molecular Biology (miscellaneous),Medicine (miscellaneous)

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1002/wsbm.1248/fullpdf

Reference110 articles.

1. Role of matricellular proteins in cardiac tissue remodeling after myocardial infarction;Matsui;World J Biol Chem,2010

2. Complement C5a, TGF-β1, and MCP-1, in sequence, induce migration of monocytes into ischemic canine myocardium within the first one to five hours after reperfusion;Birdsall;Circulation,1997

3. Neutrophil roles in left ventricular remodeling following myocardial infarction;Ma;Fibrogenesis Tissue Repair,2013

4. Classically and alternatively activated macrophages contribute to tissue remodelling after myocardial infarction;Troidl;J Cell Mol Med,2009

5. Matrix metalloproteinase-28 deletion exacerbates cardiac dysfunction and rupture after myocardial infarction in mice by inhibiting M2 macrophage activation;Ma;Circ Res,2013

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