The role of inflammatory cytokines in endothelial dysfunction

被引:410
作者
Zhang, Cuihua [1 ,2 ,3 ]
机构
[1] Univ Missouri, Dept Internal Med, Columbia, MO 65211 USA
[2] Univ Missouri, Dept Med Pharmacol & Physiol, Columbia, MO 65211 USA
[3] Univ Missouri, Dept Nutr Sci, Columbia, MO 65211 USA
关键词
inflammation; vascular dysfunction; cytokines; ischemic-heart disease; nitric oxide; vasodilation;
D O I
10.1007/s00395-008-0733-0
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Clinical and experimental data support a link between endothelial dysfunction and inflammation. Inflammatory cytokines are important protagonists in formation of atherosclerotic plaque, eliciting effects throughout the atherosclerotic vessel. Importantly, the development of atherosclerotic lesions, regardless of the risk factor, e.g., diabetes, hypertension, obesity, is characterized by disruption in normal function of the endothelial cells. Endothelial cells, which line the internal lumen of the vasculature, are part of a complex system that regulates vasodilation and vasoconstriction, growth of vascular smooth muscle cells, inflammation, and hemostasis, maintaining a proper blood supply to tissues and regulating inflammation and coagulation. Current concepts suggest that the earliest event in atherogenesis is endothelial dysfunction, manifested by deficiencies in the production of nitric oxide (NO) and prostacyclin. The focus of this review is to summarize recent evidence showing the effects of inflammation on vascular dysfunction in ischemic-heart disease, which may prompt new directions for targeting inflammation in future therapies.
引用
收藏
页码:398 / 406
页数:9
相关论文
共 70 条
[1]   Expression of NADH/NADPH oxidase p22phox in human coronary arteries [J].
Azumi, H ;
Inoue, N ;
Takeshita, S ;
Rikitake, Y ;
Kawashima, S ;
Hayashi, Y ;
Itoh, H ;
Yokoyama, M .
CIRCULATION, 1999, 100 (14) :1494-1498
[2]   PPARγ activation, by reducing oxidative stress, increases NO bioavailability in coronary arterioles of mice with Type 2 diabetes [J].
Bagi, Z ;
Koller, A ;
Kaley, G .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2004, 286 (02) :H742-H748
[3]   TNF-α antibodies are as effective as ischemic preconditioning in reducing infarct size in rabbits [J].
Belosjorow, S ;
Bolle, I ;
Duschin, A ;
Heusch, G ;
Schulz, R .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2003, 284 (03) :H927-H930
[4]   Release of TNF-α during stent implantation into saphenous vein aortocoronary bypass grafts and its relation to plaque extrusion and restenosis [J].
Boese, Dirk ;
Leineweber, Kirsten ;
Konorza, Thomas ;
Zahn, Andreas ;
Broecker-Preuss, Martina ;
Mann, Klaus ;
Haude, Michael ;
Erbel, Raimund ;
Heusch, Gerd .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2007, 292 (05) :H2295-H2299
[5]  
BUSK M, 2007, BASIC RES CARDIOL, V17, P17
[6]   Endothelial dysfunction in cardiovascular diseases - The role of oxidant stress [J].
Cai, H ;
Harrison, DG .
CIRCULATION RESEARCH, 2000, 87 (10) :840-844
[7]   Expression of nitric oxide related enzymes in coronary heart disease [J].
Chen, X. ;
Niroomand, F. ;
Liu, Z. ;
Zankl, A. ;
Katus, H. A. ;
Jahn, L. ;
Tiefenbacher, C. P. .
BASIC RESEARCH IN CARDIOLOGY, 2006, 101 (04) :346-353
[8]   Rapid reactive oxygen species production by mitochondria in endothelial cells exposed to tumor necrosis factor-α is mediated by ceramide [J].
Corda, S ;
Laplace, C ;
Vicaut, E ;
Duranteau, J .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2001, 24 (06) :762-768
[9]  
de Martin R, 2000, ARTERIOSCL THROM VAS, V20, pE83
[10]   Endothelial nitric oxide synthase activation by tumor necrosis factor α through neutral sphingomyelinase 2, sphingosine kinase 1, and sphingosine 1 phosphate receptors -: A novel pathway relevant to the pathophysiology of endothelium [J].
De Palma, C ;
Meacci, E ;
Perrotta, C ;
Bruni, P ;
Clementi, E .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2006, 26 (01) :99-105