Cross talk of the first-line defense TLRs with PI3K/Akt pathway, in preconditioning therapeutic approach.

Molecular and cellular therapies Pub Date : 2015-05-30 eCollection Date: 2015-01-01
Fatemeh Pourrajab, Mohammad Baghi Yazdi, Mojtaba Babaei Zarch, Mohammadali Babaei Zarch, Seyedhossein Hekmatimoghaddam
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引用次数: 0

Abstract

Toll-like receptor family (TLRs), pattern recognition receptors, is expressed not only on immune cells but also on non-immune cells, including cardiomyocytes, fibroblasts, and vascular endothelial cells. One main function of TLRs in the non-immune system is to regulate apoptosis. TLRs are the central mediators in hepatic, pulmonary, brain, and renal ischemic/reperfusion (I/R) injury. Up-regulation of TLRs and their ligation by either exogenous or endogenous danger signals plays critical roles in ischemia/reperfusion-induced tissue damage. Conventional TLR-NF-κB pathways are markedly activated in failing and ischemic myocardium. Recent studies have identified a cross talk between TLR activation and the PI3K/Akt pathway. The activation of TLRs is proposed to be the most potent preconditioning method after ischemia, to improve the cell survival via the mechanism involved the PI3K/Akt signaling pathway and to attenuate the subsequent TLR-NF-κB pathway stimulation. Thus, TLRs could be a great target in the new treatment approaches for myocardial I/R injury.

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一线防御tlr与PI3K/Akt通路在预处理治疗中的串扰
toll样受体家族(TLRs)是一种模式识别受体,不仅在免疫细胞上表达,也在非免疫细胞上表达,包括心肌细胞、成纤维细胞和血管内皮细胞。tlr在非免疫系统中的一个主要功能是调节细胞凋亡。tlr是肝、肺、脑和肾缺血/再灌注(I/R)损伤的中枢介质。外源性或内源性危险信号上调tlr及其结扎在缺血/再灌注诱导的组织损伤中起关键作用。常规TLR-NF-κB通路在衰竭和缺血心肌中明显激活。最近的研究发现了TLR激活和PI3K/Akt通路之间的串扰。激活TLRs被认为是缺血后最有效的预处理方法,通过参与PI3K/Akt信号通路的机制提高细胞存活,并减弱随后TLR-NF-κB通路的刺激。因此,tlr可能成为心肌I/R损伤新治疗方法的重要靶点。
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