Abstract
Toll-like receptors (TLRs), a family of surface molecules, are involved in innate immune responses. Recent studies indicated that TLRs play a critical role in inflammatory responses to exogenous and endogenous triggers. This article focuses on probable effects of TLRs in the morbidity of cardiovascular events, e.g., ischemic reperfusion (I/R) injury and atherosclerosis. TLR2 and TLR4 have been shown to have the most fundamental role in promoting cytokine production and subsequent inflammatory damages in these states. Blockade of these receptors may be beneficial in both preventing the occurrence and decreasing the complications in cardiovascular events. However, controversies exist on the certainty of this beneficial effect; therefore, additional studies are needed.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Atherosclerosis / genetics
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Atherosclerosis / immunology
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Atherosclerosis / prevention & control*
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Cytokines / biosynthesis
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Cytokines / immunology
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Gene Expression Regulation / drug effects
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Heart Failure / genetics
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Heart Failure / immunology
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Heart Failure / prevention & control*
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Humans
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Immunity, Innate / drug effects
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Immunologic Factors / pharmacology
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Immunologic Factors / therapeutic use*
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Myeloid Differentiation Factor 88 / genetics
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Myeloid Differentiation Factor 88 / immunology
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Reperfusion Injury / genetics
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Reperfusion Injury / immunology
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Reperfusion Injury / prevention & control*
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Signal Transduction / drug effects
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Toll-Like Receptor 2 / agonists
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Toll-Like Receptor 2 / antagonists & inhibitors
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Toll-Like Receptor 2 / genetics
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Toll-Like Receptor 2 / immunology*
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Toll-Like Receptor 4 / agonists
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Toll-Like Receptor 4 / antagonists & inhibitors
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Toll-Like Receptor 4 / genetics
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Toll-Like Receptor 4 / immunology*
Substances
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Cytokines
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Immunologic Factors
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MYD88 protein, human
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Myeloid Differentiation Factor 88
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TLR2 protein, human
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TLR4 protein, human
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Toll-Like Receptor 2
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Toll-Like Receptor 4