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Abstract
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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