Mechanisms of arteriogenesis

被引:85
作者
Cai, Weijun [1 ]
Schaper, Wolfgang [2 ]
机构
[1] Cent S Univ, Xiangya Sch Med, Dept Anat & Neurobiol, Changsha 410013, Hunan, Peoples R China
[2] Max Planck Inst Heart & Lung Res, Arteriogenesis Res Grp, D-61231 Bad Nauheim, Germany
关键词
arteriogenesis; shear stress; ischemic; remodeling; artery;
D O I
10.1111/j.1745-7270.2008.00436.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Patients with occlusive atherosclerotic vascular diseases have frequently developed collateral blood vessels that bypass areas of arterial obstructions. The growth of these collateral arteries has been termed "arteriogenesis", which describes the process of a small arteriole's transformation into a much larger conductance artery. In recent years, intensive investigations using various animal models have been performed to unravel the molecular mechanisms of arteriogenesis. The increasing evidence suggests that arteriogenesis seems to be triggered mainly by fluid shear stress, which is induced by the altered blood flow conditions after an arterial occlusion. Arteriogenesis involves endothelial cell activation, basal membrane degradation, leukocyte invasion, proliferation of vascular cells, neointima formation (in most species studied), changes of the extracellular matrix and cytokine participation. This paper is an in-depth review of the research critical to recent advances in the field of arteriogenesis that have provided a better understanding of its mechanisms.
引用
收藏
页码:681 / 692
页数:12
相关论文
共 113 条
[1]   Tumor necrosis factor-alpha is expressed by monocytes/macrophages following cardiac microembolization and is antagonized by cyclosporine [J].
Arras, M ;
Strasser, R ;
Mohri, M ;
Doll, R ;
Eckert, P ;
Schaper, W ;
Schaper, J .
BASIC RESEARCH IN CARDIOLOGY, 1998, 93 (02) :97-107
[2]   Arterial expansive remodeling induced by high flow rates [J].
BenDriss, A ;
Benessiano, J ;
Poitevin, P ;
Levy, BI ;
Michel, JB .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1997, 272 (02) :H851-H858
[3]   Arteriogenesis depends on circulating monocytes and macrophage accumulation and is severely depressed in op/op mice [J].
Bergmann, Caroline E. ;
Hoefer, Imo E. ;
Meder, Benjamin ;
Roth, Holger ;
van Royen, Niels ;
Breit, Sabine M. ;
Jost, Marco M. ;
Aharinejad, Seyedhossein ;
Hartmann, Susanne ;
Buschmann, Ivo R. .
JOURNAL OF LEUKOCYTE BIOLOGY, 2006, 80 (01) :59-65
[4]   EFFECTS OF EXERCISE ON COLLATERAL DEVELOPMENT IN MYOCARDIAL ISCHEMIA IN PIGS [J].
BLOOR, CM ;
WHITE, FC ;
SANDERS, TM .
JOURNAL OF APPLIED PHYSIOLOGY, 1984, 56 (03) :656-665
[5]   ACUTE VASCULAR LESIONS IN DEVELOPING CORONARY COLLATERALS [J].
BORGERS, M ;
SCHAPER, J ;
SCHAPER, W .
VIRCHOWS ARCHIV ABTEILUNG A PATHOLOGISCHE ANATOMIE, 1970, 351 (01) :1-&
[6]   Mechanical strain on osteoblasts activates autophosphorylation of focal adhesion kinase and proline-rich tyrosine kinase 2 tyrosine sites involved in ERK activation [J].
Boutahar, N ;
Guignandon, A ;
Vico, L ;
Lafage-Proust, MH .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (29) :30588-30599
[7]   Pulsatile stretch and shear stress: Physical stimuli determining the production of endothelium-derived relaxing factors [J].
Busse, R ;
Fleming, I .
JOURNAL OF VASCULAR RESEARCH, 1998, 35 (02) :73-84
[8]   Remodeling of the vascular tunica media is essential for development of collateral vessels in the canine heart [J].
Cai, WJ ;
Kocsis, E ;
Wu, XQ ;
Rodríguez, M ;
Luo, XG ;
Schaper, W ;
Schaper, J .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 2004, 264 (1-2) :201-210
[9]   Presence of Cx37 and lack of desmin in smooth muscle cells are early markers for arteriogenesis [J].
Cai, WJ ;
Kocsis, E ;
Scholz, D ;
Luo, XG ;
Schaper, W ;
Schaper, J .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 2004, 262 (1-2) :17-23
[10]   Remodeling of the adventitia during coronary arteriogenesis [J].
Cai, WJ ;
Koltai, S ;
Kocsis, E ;
Scholz, D ;
Kostin, S ;
Luo, XG ;
Schaper, W ;
Schaper, J .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2003, 284 (01) :H31-H40