Innate immunity and cardiomyocytes in ischemic heart disease

Research output: Contribution to journalArticle

39 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalLife Sciences
Volume100
Issue number1
DOIs
StatePublished - Mar 28 2014

Fingerprint

Pattern Recognition Receptors
Cardiac Myocytes
Innate Immunity
Myocardial Ischemia
Reperfusion Injury
Toll-Like Receptors
Heat-Shock Proteins
Myocardial Reperfusion Injury
Myocardial Reperfusion
Ischemia
Inflammation

Keywords

  • Cardiomyocytes
  • Heart
  • Inflammation
  • Innate immunity
  • Ischemia/reperfusion
  • NF-κB
  • Pattern recognition receptor
  • TLR2
  • TLR4

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Innate immunity and cardiomyocytes in ischemic heart disease. / Lin, Li; Knowlton, Anne A.

In: Life Sciences, Vol. 100, No. 1, 28.03.2014, p. 1-8.

Research output: Contribution to journalArticle

@article{0e76e38e763a4065b1404564b448dc35,
title = "Innate immunity and cardiomyocytes in ischemic heart disease",
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.",
keywords = "Cardiomyocytes, Heart, Inflammation, Innate immunity, Ischemia/reperfusion, NF-κB, Pattern recognition receptor, TLR2, TLR4",
author = "Li Lin and Knowlton, {Anne A}",
year = "2014",
month = "3",
day = "28",
doi = "10.1016/j.lfs.2014.01.062",
language = "English (US)",
volume = "100",
pages = "1--8",
journal = "Life Sciences",
issn = "0024-3205",
publisher = "Elsevier Inc.",
number = "1",

}

TY - JOUR

T1 - Innate immunity and cardiomyocytes in ischemic heart disease

AU - Lin, Li

AU - Knowlton, Anne A

PY - 2014/3/28

Y1 - 2014/3/28

N2 - 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.

AB - 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.

KW - Cardiomyocytes

KW - Heart

KW - Inflammation

KW - Innate immunity

KW - Ischemia/reperfusion

KW - NF-κB

KW - Pattern recognition receptor

KW - TLR2

KW - TLR4

UR - http://www.scopus.com/inward/record.url?scp=84896488646&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84896488646&partnerID=8YFLogxK

U2 - 10.1016/j.lfs.2014.01.062

DO - 10.1016/j.lfs.2014.01.062

M3 - Article

C2 - 24486305

AN - SCOPUS:84896488646

VL - 100

SP - 1

EP - 8

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

IS - 1

ER -