Extracellular Heat Shock Protein 70 Induces Cardiomyocyte Inflammation and Contractile Dysfunction via TLR2
Author:
Affiliation:
1. Critical Care Research Laboratories, Heart+Lung Institute at St. Paul's Hospital, University of British Columbia
Publisher
Japanese Circulation Society
Subject
Cardiology and Cardiovascular Medicine,General Medicine
Link
https://www.jstage.jst.go.jp/article/circj/75/10/75_CJ-11-0194/_pdf
Reference50 articles.
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2. 2. Boyd JH, Kan B, Roberts H, Wang Y, Walley KR. S100A8 and S100A9 mediate endotoxin-induced cardiomyocyte dysfunction via the receptor for advanced glycation end products. Circ Res 2008; 102: 1239-1246.
3. 3. Shiono T, Kodama M, Hanawa H, Fuse K, Yamamoto T, Aizawa Y. Suppression of myocardial inflammation using suramin, a growth factor blocker. Circ J 2002; 66: 385-389.
4. 4. Yasue H, Hirai N, Mizuno Y, Harada E, Itoh T, Yoshimura M, et al. Low-grade inflammation, thrombogenicity, and atherogenic lipid profile in cigarette smokers. Circ J 2006; 70: 8-13.
5. 5. Date T, Yamashita T, Sekiguchi A, Iwasaki YK, Aizawa T, Yamane T, et al. Infiltration of macrophages through the atrial endocardium of inflammation-induced rats: Contribution of fractalkine. Circ J 2009; 73: 932-937.
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