期刊
CELLULAR AND MOLECULAR LIFE SCIENCES
卷 70, 期 16, 页码 2859-2872出版社
SPRINGER BASEL AG
DOI: 10.1007/s00018-012-1194-z
关键词
Atherosclerosis; Oxidized LDL; LOX-1; Soluble LOX-1; Review
资金
- National Natural Science Foundation of China [81072641]
- NSFC-CIHR CHINA-CANADA Joint Health Research Initiative Proposal [30811120434]
- National Science and Technology Major Project of China Key New Drug Creation and Manufacturing Program'' [2009ZX09102-152, 2011ZX09401-307]
- Natural Science Foundation of Guangdong Province [S2011030003190]
- Major Project of Guangdong Province [2008A030201013, 2012A080201007]
- Major Project of Department of Education of Guangdong Province [CXZD1006]
- National Health and Medical Research Council of Australia
- National Heart Foundation of Australia
- Diabetes Australia Research Trust
- Ministry of Education of China
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [ZIAHL002541] Funding Source: NIH RePORTER
Lectin-like oxidized LDL (oxLDL) receptor-1 (LOX-1, also known as OLR-1), is a class E scavenger receptor that mediates the uptake of oxLDL by vascular cells. LOX-1 is involved in endothelial dysfunction, monocyte adhesion, the proliferation, migration, and apoptosis of smooth muscle cells, foam cell formation, platelet activation, as well as plaque instability; all of these events are critical in the pathogenesis of atherosclerosis. These LOX-1-dependent biological processes contribute to plaque instability and the ultimate clinical sequelae of plaque rupture and life-threatening tissue ischemia. Administration of anti-LOX-1 antibodies inhibits atherosclerosis by decreasing these cellular events. Over the past decade, multiple drugs including naturally occurring antioxidants, statins, antiinflammatory agents, antihypertensive and antihyperglycemic drugs have been demonstrated to inhibit vascular LOX-1 expression and activity. Therefore, LOX-1 represents an attractive therapeutic target for the treatment of human atherosclerotic diseases. This review aims to integrate the current understanding of LOX-1 signaling, regulation of LOX-1 by vasculoprotective drugs, and the importance of LOX-1 in the pathogenesis of atherosclerosis.
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