Singh Madhu V, Abboud François M
Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa; Abboud Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, Iowa; and
Department of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa; Abboud Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, Iowa; and Department of Molecular Physiology and Biophysics, University of Iowa, Iowa City, Iowa.
Am J Physiol Regul Integr Comp Physiol. 2014 Sep 1;307(5):R501-4. doi: 10.1152/ajpregu.00194.2014. Epub 2014 Jun 11.
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.
高血压以及加速心血管损伤的相关炎症过程受先天免疫系统调控。Toll样受体(TLR)是先天免疫系统的主要组成部分,可识别内源性损伤相关分子模式,以激活包括核因子-κB(NF-κB)激活在内的显著炎症信号。然而,TLR在高血压病因学中的作用尚未完全明确。TLR信号传导依赖于衔接蛋白,这些衔接蛋白与TLR表达模式一起赋予炎症反应及其病理靶点特异性。在此,我们综述了TLR及其衔接蛋白如何通过不同刺激差异影响高血压和心脏肥大的概念框架。