The crossroads of inflammation, fibrosis, and arrhythmia following myocardial infarction-Reference-Cited by-同舟云学术

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The crossroads of inflammation, fibrosis, and arrhythmia following myocardial infarction

Published:2016-02 Issue: Volume:91 Page:114-122
ISSN:0022-2828
Container-title:Journal of Molecular and Cellular Cardiology
language:en
Short-container-title:Journal of Molecular and Cellular Cardiology

Author:

Francis Stuart Samantha D.,De Jesus Nicole M.,Lindsey Merry L.,Ripplinger Crystal M.

Funder

National Institutes of Health

American Heart Association

Biomedical Laboratory Research and Development Service

Publisher

Elsevier BV

Subject

Cardiology and Cardiovascular Medicine,Molecular Biology

Reference90 articles.

1. The inflammatory response in myocardial injury, repair, and remodelling;Frangogiannis;Nat. Rev. Cardiol.,2014

2. Macrophage roles following myocardial infarction;Lambert;Int. J. Cardiol.,2008

3. CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory T cells;Dobaczewski;Am. J. Pathol.,2010

4. The chemokine decoy receptor D6 prevents excessive inflammation and adverse ventricular remodeling after myocardial infarction;Cochain;Arterioscler. Thromb. Vasc. Biol.,2012

5. Early matrix metalloproteinase-12 inhibition worsens post-myocardial infarction cardiac dysfunction by delaying inflammation resolution;Iyer;Int. J. Cardiol.,2015

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