Abstract
The heart possesses an innate immune system that is intended to delimit tissue injury, as well as orchestrate homoeostatic responses that enable myocardial repair. The extant literature suggests that this intrinsic stress response system is mediated, at least in part, by a family of pattern recognition receptors, most notably the Toll-like receptors. Although the innate immune system provides a short-term adaptive response to tissue injury, the beneficial effects of this phylogenetically ancient system may be lost if innate immune signaling becomes sustained and/or excessive, in which case, the salutary effects of activation of these pathways are contravened by the known deleterious effects of inflammatory signaling. In this chapter, we review the biology of innate immune signaling in the heart with a focus on the biology of and innate immune receptors, as well as proinflammatory cytokines and innate immune receptors, chemokines, and leukocytes. This chapter also discusses how activation of the innate immune system with the subsequent elaboration of inflammatory cytokines plays an important role in the progression of heart failure, by virtue of the deleterious effects that these molecules exert on the heart and the peripheral circulation.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call