MicroRNA profiling in patients with coronary artery disease.

本研究研究了与内皮细胞损伤和血管炎症有关的microRNA生物学，如Toll样受体4(TLR4)。内皮祖细胞在维持血管完整性方面发挥着重要作用。MiR-221/222是一类新发现的小RNA，其生理作用与内皮祖细胞的增殖密切相关。此外，本研究还表明，阿托伐他汀降脂治疗(LLT)可增加冠心病患者的EPC数量，降低miR-221/222水平，这可能是LLT与阿托伐他汀联合治疗冠心病的有益效果之一。Let-7家族microRNAs中的let-7i直接调节Toll样受体4(TLR4)的表达，参与免疫应答。MiR-146a/b调控TLR4下游分子(IRAK1和TRAF6)。本研究表明，在冠心病患者中miR-146a/b以TLR4信号表达，他汀类药物和RAS拮抗剂联合治疗可能会影响这些水平。此外，在冠心病患者中，LET-7i对TLR4起负调节作用，而阿托伐他汀通过LET-7影响TLR4水平。本研究表明，ARB和阿托伐他汀治疗降低了冠心病患者的miR-146a/b和TLR4信号，这可能是ARB和他汀类药物抗动脉粥样硬化的作用之一。

The present study has investigated microRNA biology concerning endothelial cellular injury and vascular inflammation, such as Toll-like receptor 4 (TLR4). Endothelial progenitor cells (EPCs) play an important role in the maintenance of vascular integrity. The physiological role of miR-221/222, a newly discovered class of small RNA, is closely linked to the proliferation of EPCs. In addition,this study demonstrates that lipid lowering therapy (LLT) with atorvastatin increases EPC numbers and decreases miR-221/222 levels in patients with CAD, possibly contributing to the beneficial effects of LLT with atorvastatin in this disorder.TLR4 signal plays an important role in immunity in CAD. One of the let-7 family microRNAs, let-7i, directly regulates Toll-like receptor 4 (TLR4) expression and contributes to immune response. The miR-146a / b regulates TLR4 downstream molecules (IRAK1 and TRAF6). The present study has shown that miR-146a / b were expressed with TLR4 signal in CAD patients, and combined treatment with a statin and RAS blockade might affect these levels. In addition, let-7i played a negative regulator of TLR4 in patients with CAD, and atorvastatin affected TLR4 levels via let-7i.This study demonstrates that treatment with ARB and atrovastatin decreases miR-146a / b and TLR4 signal in patients with CAD, possibly contributing to the anti-atherogenic effects of ARB and statins in this disorder.