Toll-like receptors and hypertension

Abstract

Hypertension and associated inflammatory processes that accelerate cardiovascular damage are regulated by the innate immune system. Toll-like receptors (TLR) are major components of the innate immune system that recognize endogenous damage-associated molecular patterns to activate prominent inflammatory signaling including activation of nuclear factor-κB (NF-κB). However, the role of TLR in the etiology of hypertension is not well understood. TLR signaling is dependent on adaptor proteins that, along with the TLR expression patterns, confer specificity of the inflammatory response and its pathological targets. Here we review the conceptual framework of how TLR and their adaptor proteins may differentially affect hypertension and cardiac hypertrophy by different stimuli.

Keywords: MyD88; hypertension; innate immune system; toll-like receptors.

Fig. 1.

Pathways of Toll-like receptors (TLR) in hypertension and cardiac hypertrophy. A: myocardial infarction (MI)-induced cardiac hypertrophy and ANG II-induced hypertension and cardiac hypertrophy through intact TLR pathways in the wild type (WT). B: MI-induced cardiac hypertrophy is dependent on the major TLR adaptor protein myeloid differentiation factor 88 (MyD88) but ANG II-induced hypertension and hypertrophy are not. C: MyD88-independent pathways may regulate ANG II-induced cardiac hypertrophy and hypertension.