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Innate Immunity and Cardiomyocytes in Ischemic Heart Disease

Overview
Journal Life Sci
Publisher Elsevier
Date 2014 Feb 4
PMID 24486305
Citations 36
Authors
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Abstract

Myocardial ischemia/reperfusion (I/R) is the most common cause of myocardial inflammation, which is primarily a manifestation of the innate immune responses. Innate immunity is activated when pattern recognition receptors (PRRs) respond to molecular patterns common to microbes and to danger signals expressed by injured or infected cells, so called pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). The expression of various PRRs in cardiomyocytes and the release of DAMPs from cardiomyocytes subjected to I/R injury, through active mechanisms as well as passive processes, enable cardiomyocytes to generate innate immune responses. Studies in isolated heart and cardiomyocytes have confirmed the inflammatory and functional effects of cardiac PRRs especially Toll-like receptors in response to I/R-derived DAMPs, such as heat shock proteins. This review addresses the active role of cardiomyocytes in mediating innate inflammatory responses to myocardial I/R. We propose that cardiomyocytes act as innate immune cells in myocardial I/R injury.

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References
1.
Villarreal-Calderon R, Dale G, Delgado-Chavez R, Torres-Jardon R, Zhu H, Herritt L . Intra-city Differences in Cardiac Expression of Inflammatory Genes and Inflammasomes in Young Urbanites: A Pilot Study. J Toxicol Pathol. 2012; 25(2):163-73. PMC: 3392908. DOI: 10.1293/tox.25.163. View

2.
Lancaster G, Febbraio M . Exosome-dependent trafficking of HSP70: a novel secretory pathway for cellular stress proteins. J Biol Chem. 2005; 280(24):23349-55. DOI: 10.1074/jbc.M502017200. View

3.
Mason D, Beck P, Muruve D . Nucleotide-binding oligomerization domain-like receptors and inflammasomes in the pathogenesis of non-microbial inflammation and diseases. J Innate Immun. 2011; 4(1):16-30. DOI: 10.1159/000334247. View

4.
Baumgarten G, Knuefermann P, Schuhmacher G, Vervolgyi V, von Rappard J, Dreiner U . Toll-like receptor 4, nitric oxide, and myocardial depression in endotoxemia. Shock. 2005; 25(1):43-9. DOI: 10.1097/01.shk.0000196498.57306.a6. View

5.
Ha T, Hua F, Liu X, Ma J, McMullen J, Shioi T . Lipopolysaccharide-induced myocardial protection against ischaemia/reperfusion injury is mediated through a PI3K/Akt-dependent mechanism. Cardiovasc Res. 2008; 78(3):546-53. DOI: 10.1093/cvr/cvn037. View