Toll-like receptor signaling in the ischemic heart.
Toll-like receptors (TLRs) have been identified as primary innate immune receptors. They distinguish among different patterns of pathogens and rapidly activate an innate immune response. However, TLRs can also be stimulated by host-derived molecules. TLRs are expressed in the cardiovascular system and could thus be a key link between cardiovascular diseases and the immune system. Increasing evidence suggests that TLR signaling promotes injury in the heart after ischemia, ischemia/reperfusion or hypertrophic stimuli. Herein we review the experimental and clinical evidence for the involvement of TLR and its downstream signaling molecules in cardiac ischemic injury.
Medizinische Klinik und Poliklinik I, Herzkreislauf-Zentrum, Universitätsklinikum Würzburg, Würzburg, Germany. frantz_s@medizin.uni-wuerzburg.de
Stefan
S
Frantz
Georg
G
Ertl
Johann
J
Bauersachs
D000818:Animals; D006332:Cardiomegaly / Q000503:physiopathology; D004195:Disease Models, Animal; D006333:Heart Failure / Q000503:physiopathology; D006801:Humans; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015427:Reperfusion Injury / Q000503:physiopathology; D015398:Signal Transduction / Q000502:physiology*; D051195:Toll-Like Receptor 2 / Q000502:physiology; D051197:Toll-Like Receptor 4 / Q000502:physiology; D051193:Toll-Like Receptors / Q000502:physiology*
C495342:TLR2 protein, human; C495345:TLR4 protein, human; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors