eNOS, metabolic syndrome and cardiovascular disease

被引:274
作者
Huang, Paul L. [1 ,2 ,3 ]
机构
[1] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA
[2] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA
[3] Harvard Univ, Sch Med, Boston, MA 02114 USA
关键词
ENDOTHELIAL NITRIC-OXIDE; INSULIN-RESISTANCE; MITOCHONDRIAL BIOGENESIS; SYNTHASE PHOSPHORYLATION; ACCELERATED ATHEROSCLEROSIS; MICROVASCULAR DYSFUNCTION; PRIMARY PREVENTION; PROVISIONAL REPORT; ADIPOSE-TISSUE; MICE LACKING;
D O I
10.1016/j.tem.2009.03.005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Large epidemiologic studies have established that diabetes, hyperlipidemia and obesity all increase the risk for cardiovascular disease. However, the precise mechanisms by which these metabolic disorders increase the propensity to develop atherosclerosis are not known. Recently, the concept of the metabolic syndrome - a constellation of conditions including obesity, hypertension, hyperlipidemia and insulin resistance - has received much attention. Studies on the metabolic syndrome might enable a better understanding of the underlying biological mechanisms that lead to cardiovascular disease. This review focuses on endothelial nitric oxide synthase and summarizes evidence that a reduction in the bioavailability of endothelium-derived nitric oxide serves as a key link between metabolic disorders and cardiovascular risk.
引用
收藏
页码:295 / 302
页数:8
相关论文
共 89 条
[1]  
Alberti KGMM, 1998, DIABETIC MED, V15, P539, DOI 10.1002/(SICI)1096-9136(199807)15:7<539::AID-DIA668>3.0.CO
[2]  
2-S
[3]   Nitric oxide synthases: structure, function and inhibition [J].
Alderton, WK ;
Cooper, CE ;
Knowles, RG .
BIOCHEMICAL JOURNAL, 2001, 357 (03) :593-615
[4]   CLOSE RELATION OF ENDOTHELIAL FUNCTION IN THE HUMAN CORONARY AND PERIPHERAL CIRCULATIONS [J].
ANDERSON, TJ ;
UEHATA, A ;
GERHARD, MD ;
MEREDITH, IT ;
KNAB, S ;
DELAGRANGE, D ;
LIEBERMAN, EH ;
GANZ, P ;
CREAGER, MA ;
YEUNG, AC ;
SELWYN, AP .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1995, 26 (05) :1235-1241
[5]  
Balkau B, 1999, DIABETIC MED, V16, P442
[6]   Endothelial dysfunction and atherosclerosis: Endothelin receptor antagonists as novel therapeutics [J].
Barton M. .
Current Hypertension Reports, 2000, 2 (1) :84-91
[7]  
Beckman JS, 1996, AM J PHYSIOL-CELL PH, V271, pC1424
[8]   Leptin decreases plasma paraoxonase 1 (PON1) activity and induces oxidative stress: the possible novel mechanism for proatherogenic effect of chronic hyperleptinemia [J].
Beltowski, J ;
Wojcicka, G ;
Jamroz, A .
ATHEROSCLEROSIS, 2003, 170 (01) :21-29
[9]   Adipose tissue, inflammation, and cardiovascular disease [J].
Berg, AH ;
Scherer, PE .
CIRCULATION RESEARCH, 2005, 96 (09) :939-949
[10]   Flow-dependent regulation of endothelial nitric oxide synthase: role of protein kinases [J].
Boo, YC ;
Jo, H .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2003, 285 (03) :C499-C508