Innate immunity and cardiomyocytes in ischemic heart disease

LIFE SCIENCES

卷:100

Review

Lin, Li¹  Knowlton, Anne A.^2,3,4,5 

[1] Second Mil Med Univ, Dept Physiol, Shanghai 200433, Peoples R China

[2] Univ Calif Davis, Davis, CA 95616 USA

[3] Univ Calif Davis, Dept Med, Davis, CA 95616 USA

[4] Univ Calif Davis, Dept Pharmacol, Davis, CA 95616 USA

[5] Northern Calif VA, Sacramento, CA USA

关键词: Heart;    Cardiomyocytes;    Pattern recognition receptor;    Innate immunity;    Inflammation;    Ischemia/reperfusion;    TLR4;    TLR2;    NF-kappa B;   

DOI  :  10.1016/j.lfs.2014.01.062

来源: Elsevier

【 摘 要 】

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. Published by Elsevier Inc.

【 授权许可】

Free