Department of Cardiology, the First College of Clinical Medical Science, Yichang Central People's Hospital, China Three Gorges University, Yichang, 443000, China.
Curr Med Sci. 2019 Apr;39(2):185-189. doi: 10.1007/s11596-019-2017-3. Epub 2019 Apr 23.
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.
Raidoprotective 105 (RP105) 最初在小鼠 B 细胞表面被发现,现已证实 RP105 可作为心血管疾病 (CVD) 中的炎症调节剂,如心肌缺血再灌注损伤 (MI/RI)、动脉粥样硬化和心肌梗死 (MI)。作为 Toll 样受体 (TLR) 同源物的一员,RP105 能够调节 Toll 样受体 (TLR4) 信号通路,参与多种生物学过程。越来越多的证据表明,RP105 调节 TLR4 和磷酸肌醇 3-激酶 (PI3K) 信号通路的功能。在这里,我们通过调节 TLR4/PI3K 信号通路来综述 RP105 对 CVD 的影响。