The Role of RP105 in Cardiovascular Disease through Regulating TLR4 and PI3K Signaling Pathways

The Role of RP105 in Cardiovascular Disease through Regulating TLR4 and PI3K Signaling Pathways
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RP105 通过调节 TLR4 和 PI3K 信号通路在心血管疾病中的作用

DOI:
10.1007/s11596-019-2017-3
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发表时间:
2019-04
影响因子:
2.4
通讯作者:
Zhi-xing FAN
Zhi-xing FAN
中科院分区:
医学3区
文献类型:
--
作者:
Jian YANG;Ping ZENG;Jun YANG;Zhi-xing FAN

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RP 105(Raidoprotective 105)是在小鼠B细胞表面发现的一种新型的抗炎因子,在心血管疾病如心肌缺血再灌注损伤(MI/RI)、动脉粥样硬化和心肌梗死(MI)中具有重要的抗炎作用。RP 105作为Toll样受体(TLR)的一个成员,参与多种生物学过程,并能调控Toll样受体(TLR 4)信号通路。越来越多的证据表明,RP 105调节TLR 4和磷脂酰肌醇3-激酶(PI 3 K)信号通路的功能。本文就RP 105通过调节TLR 4/PI 3 K信号通路对CVD的影响作一综述。
Raidoprotective 105 (RP105) was first discovered on the surface of mouse B cells and it has been demonstrated that RP105 can function as an inflammatory regulator in cardiovascular disease (CVD), such as myocardial ischemic reperfusion injury (MI/RI), atherosclerosis and myocardial infarction (MI). As a member of Toll-like receptor (TLR) homolog which is capable of regulating toll-like receptor (TLR4) signaling pathway, RP105 is implicated in various biological processes. Mounting evidence suggests that RP105 regulates the function of TLR4 and phosphoinositide 3-kinase (PI3K) signaling pathways. Here, we review the effect of RP105 on CVD through regulating TLR4/PI3K signaling pathways.
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