LOX-1, oxidant stress, mtDNA damage, autophagy, and immune response in atherosclerosis

被引：63

作者：

Ding, Zufeng ^{[1
,2
,3
]}

Liu, Shijie ^{[1
,2
]}

Wang, Xianwei ^{[1
,2
]}

Dai, Yao ^{[1
,2
]}

Khaidakov, Magomed ^{[1
,2
]}

Romeo, Francesco ^{[4
]}

Mehta, Jawahar L. ^{[1
,2
]}

机构：

[1] Cent Arkansas Vet Healthcare Syst, Little Rock, AR 72212 USA

[2] Univ Arkansas Med Sci, Dept Med, Little Rock, AR 72212 USA

[3] Beihang Univ, Sch Biol Sci & Med Engn, Minist Educ, Key Lab Biomech & Mechanobiol, Beijing 100191, Peoples R China

[4] Univ Rome, Rome, Italy

来源：

CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY | 2014年 / 92卷 / 07期

基金：

中国国家自然科学基金; 高等学校博士学科点专项科研基金;

关键词：

LOX-1; mitochondrial DNA; autophagy; immunity; atherosclerosis; reactive oxygen species; oxidized LDL; LOW-DENSITY-LIPOPROTEIN; ARTERY ENDOTHELIAL-CELLS; MITOCHONDRIAL-DNA DAMAGE; OXIDIZED LDL; OX-LDL; APOPTOSIS; RECEPTOR; MECHANISMS; INFLAMMATION; DYSFUNCTION;

D O I：

10.1139/cjpp-2013-0420

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

As a major receptor for oxidized low density lipoprotein (ox-LDL), lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is upregulated in many pathophysiological events, including endothelial cell dysfunction and smooth muscle cell growth, as well as monocyte migration and transformation into foam cells, which are present in atherosclerosis and myocardial ischemia. Excessive production of reactive oxygen species (ROS) increases LOX-1 expression, induces mitochondrial DNA damage, and activates autophagy. Damaged mitochondrial DNA that escapes from autophagy induces an inflammatory response. This paper reviews the potential link between LOX-1, mitochondrial DNA damage, autophagy, and immune response in atherosclerosis.

引用

页码：524 / 530

页数：7

共 34 条

[1]

Structure and chromosomal assignment of the human lectin-like oxidized low-density-lipoprotein receptor-1 (LOX-1) gene [J].