Abstract
Toll-like receptors (TLRs) are a member of the innate immune system. TLRs detect invading pathogens through the pathogen-associated molecular patterns (PAMPs) recognition and play an essential role in the host defense. TLRs can also sense a large number of endogenous molecules with the damage-associated molecular patterns (DAMPs) that are produced under various injurious conditions. Animal studies of the last decade have demonstrated that TLR signaling contributes to the pathogenesis of the critical cardiac conditions, where myocardial inflammation plays a prominent role, such as ischemic myocardial injury, myocarditis, and septic cardiomyopathy. This paper reviews the animal data on (1) TLRs, TLR ligands, and the signal transduction system and (2) the important role of TLR signaling in these critical cardiac conditions.
Highlights
Innate immune system represents the first line of defense against foreign pathogens
In a rat model of I/R injury, Hua and colleagues reported that adenoviral expression of dn-MyD88 three days prior to the onset of myocardial ischemia led to reduced infarct sizes and attenuated NF-κB activity, consistent with the notion that MyD88 signaling may contribute to ischemic myocardial injury by attenuating inflammatory response that is dependent on NF-κB signaling
A wide variety of microbial and nonmicrobial Toll-like receptors (TLRs) ligands have been identified. These ligands act through their respective TLRs and elicit a variety of biochemical and proinflammatory responses via the distinct intracellular signal transduction systems
Summary
Innate immune system represents the first line of defense against foreign pathogens. Toll-like receptors (TLRs) belong to the family of pattern recognition receptors (PRRs). PRRs recognize the conserved motifs in pathogens termed pathogen-associated molecular patterns (PAMPs) and trigger innate immune response [1, 2]. In addition to participating in the host defense against infectious pathogens, accumulating evidence suggests that TLRs play an essential role in tissue inflammationand contribute to “noninfectious” tissue damage such as cardiac ischemia/reperfusion (I/R) injury, postischemic remodeling, and atherosclerosis [3,4,5,6]. This paper reviews TLR signaling and its critical roles in several inflammatory cardiac conditions: I/R injury, viral and autoimmune myocarditis, and septic cardiomyopathy
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