Innate immunity and cardiomyocytes in ischemic heart disease

Life Sci. 2014 Mar 28;100(1):1-8. doi: 10.1016/j.lfs.2014.01.062. Epub 2014 Jan 28.


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.

Keywords: Cardiomyocytes; Heart; Inflammation; Innate immunity; Ischemia/reperfusion; NF-κB; Pattern recognition receptor; TLR2; TLR4.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • HMGB1 Protein / physiology
  • Heat-Shock Proteins / physiology
  • Humans
  • Immunity, Innate*
  • Lectins, C-Type / physiology
  • Myocardial Reperfusion Injury / immunology*
  • Myocardial Reperfusion Injury / metabolism
  • Myocardium / immunology
  • Myocardium / metabolism
  • Myocardium / pathology
  • Myocytes, Cardiac / immunology
  • Myocytes, Cardiac / metabolism*
  • Nod Signaling Adaptor Proteins / physiology
  • Toll-Like Receptors / physiology


  • HMGB1 Protein
  • Heat-Shock Proteins
  • Lectins, C-Type
  • Nod Signaling Adaptor Proteins
  • Toll-Like Receptors