Effect of statins on toll-like receptors: a new insight to pleiotropic effects

被引：152

作者：

Bahrami, Afsane ^{[1
]}

Parsamanesh, Negin ^{[2
]}

Atkin, Stephen L. ^{[3
]}

Banach, Maciej ^{[4
,5
]}

Sahebkar, Amirhossein ^{[6
,7
,8
]}

机构：

[1] Birjand Univ Med Sci, Cellular & Mol Res Ctr, Birjand, Iran

[2] Birjand Univ Med Sci, Student Res Comm, Birjand, Iran

[3] Weill Cornell Med Qatar, Doha, Qatar

[4] Med Univ Lodz, WAM Univ Hosp Lodz, Dept Hypertens, Zeromskiego 113, Lodz, Poland

[5] PMMHRI, Lodz, Poland

[6] Mashhad Univ Med Sci, Neurogen Inflammat Res Ctr, Mashhad, Iran

[7] Mashhad Univ Med Sci, Pharmaceut Technol Inst, Biotechnol Res Ctr, Mashhad, Iran

[8] Mashhad Univ Med Sci, Sch Pharm, Mashhad, Iran

来源：

PHARMACOLOGICAL RESEARCH | 2018年 / 135卷

关键词：

HMG-CoA reductase; TLR; Inflammation; Atherosclerosis; Statins; KAPPA-B ACTIVATION; VASCULAR SMOOTH-MUSCLE; CORONARY-HEART-DISEASE; RHEUMATOID-ARTHRITIS; TOLL-LIKE-RECEPTOR-4; EXPRESSION; SIGNALING PATHWAY; ATHEROSCLEROTIC PLAQUES; INFLAMMATORY MEDIATORS; CYTOKINE PRODUCTION; ENDOGENOUS LIGANDS;

D O I：

10.1016/j.phrs.2018.08.014

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

The toll-like receptors (TLRs) are a class of transmembrane-spanning receptors that are sentinels of both innate and adaptive immunity. Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are the most commonly prescribed therapeutic agents for treating hypercholesterolemia globally. However, statin therapy appears to have pleiotropic effects including attenuation of chronic low-grade inflammation and modulation of TLR activity. Statins through abolition of TLR4 expression and regulation of the TLR4/Myd88/NF-kappa B signaling pathway may slow the progression of atherosclerosis and other inflammatory diseases. In this review, we have focused on the impact and mechanism of action of statins on cardiovascular and non-cardiovascular diseases.

引用

页码：230 / 238

页数：9

共 136 条

[1]

Innate immunity and toll-like receptors: Clinical implications of basic science research [J].