Toll-like receptors (TLR) are key pattern recognition receptors in the innate immune system. The TLR-mediated immune response against pathogens is usually protective however inappropriate TLR activation may lead to excessive tissue damage. It is well recognised that TLRs respond to a variety of endogenous as well as exogenous ligands. By responding to endogenous ligands that are exposed during cellular damage, TLRs have been implicated in a range of pathological conditions associated with cardiovascular dysfunction. Increasing knowledge on the mechanisms involved in TLR signalling has encouraged the exploration of therapeutic pharmacological modulation of TLR activation in conditions such as atherosclerosis, ischaemic heart disease, heart failure and ischaemic reperfusion injury. The aim of this review is to explore the translational potentials of TLR modification in cardiovascular dysfunction, where these agents have been studied.
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