title: Innate immune signaling in cardiac ischemia.
abstract: Despite advances in treatment of patients who suffer from ischemic heart disease, morbidity related to myocardial infarction is increasing in Western societies. Acute and chronic immune responses elicited by myocardial ischemia have an important role in the functional deterioration of the heart. Research on modulation of the inflammatory responses was focused on effector mediators such as leukocytes. However, increasing evidence indicates that various endogenous ligands that act as 'danger signals', also called danger-associated molecular patterns (DAMPs), are released upon injury and modulate inflammation. Originally described as part of the first-line defense against invading microorganisms, several Toll-like receptors (TLRs) on leukocytes and parenchymal cells have now been shown to respond to such signals and to have a pivotal role in noninfectious pathological cardiovascular conditions, such as ischemia-reperfusion injury and heart failure. From a therapeutic perspective, DAMPs are attractive targets owing to their specific induction after injury. In this Review, we will discuss innate immune activation through TLRs in cardiac ischemia mediated by DAMPs.
authors: University Medical Center Utrecht, Laboratory of Experimental Cardiology, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
authors: Fatih
authors: F
authors: Arslan
authors: Dominique P
authors: DP
authors: de Kleijn
authors: Gerard
authors: G
authors: Pasterkamp
mesh_terms: D000818:Animals; D006801:Humans; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000378:metabolism; D017202:Myocardial Ischemia / Q000276:immunology*; D009206:Myocardium / Q000276:immunology*; D051192:Receptors, Pattern Recognition / Q000378:metabolism; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D018836:Inflammation Mediators; D051192:Receptors, Pattern Recognition; D051193:Toll-Like Receptors