Arterial adaptations to chronic changes in haemodynamic function: Coupling vasomotor tone to structural remodelling

被引:73
作者
Dajnowiec, Dorota
Langille, B. Lowell
机构
[1] Univ Toronto, Hlth Network, Toronto Gen Res Inst, Toronto, ON M5G 2C4, Canada
[2] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON M5G 1L5, Canada
关键词
arterial remodelling; entrenchment; haemodynamic function; hypertension; shear stress; vasoconstriction; vascular tone;
D O I
10.1042/CS20060337
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Healthy mature arteries are usually extremely quiescent tissues with cell proliferation rates much below I %/day and with extracellular matrix constituents exhibiting half-lives of years to decades. However, chronic physiological or pathological changes in haemodynamic function elicit arterial remodelling processes that may involve substantial tissue synthesis, degradation or turnover. Although these remodelling processes accommodate changing demands placed upon the cardiovascular system by physiological adaptations, they can compromise further perfusion in the context of arterial occlusive disease and they entrench hypertension and may exacerbate its progression. Recent findings indicate that some of the most important such remodelling responses involve the integrated effects of persistently altered vascular tone that feed into restructuring responses, with common signalling pathways frequently interacting in the control of both phases of the response. Current efforts to define these signals and their targets may provide new directions for therapeutic interventions to treat important vascular disorders.
引用
收藏
页码:15 / 23
页数:9
相关论文
共 76 条
[1]  
Akimov SS, 2001, J CELL SCI, V114, P2989
[2]   Small artery remodeling depends on tissue-type transglutaminase [J].
Bakker, ENTP ;
Buus, CL ;
Spaan, JAE ;
Perree, J ;
Ganga, A ;
Rolf, TM ;
Sorop, O ;
Bramsen, LH ;
Mulvany, MJ ;
VanBavel, E .
CIRCULATION RESEARCH, 2005, 96 (01) :119-126
[3]   Flow-dependent remodeling of small arteries in mice deficient for tissue-type transglutaminase - Possible compensation by macrophage-derived factor XIII [J].
Bakker, Erik N. T. P. ;
Pistea, Adrian ;
Spaan, Jos A. E. ;
Rolf, Titia ;
de Vries, Carlie J. ;
van Rooijen, Nico ;
Candi, Eleonara ;
VanBavel, Ed .
CIRCULATION RESEARCH, 2006, 99 (01) :86-92
[4]   Analysis of tissue transglutaminase function in the migration of swiss 3T3 fibroblasts - The active-state conformation of the enzyme does not affect cell motility but is important for its secretion [J].
Balklava, Z ;
Verderio, E ;
Collighan, R ;
Gross, S ;
Adams, J ;
Griffin, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (19) :16567-16575
[5]   Dwarf galaxies captured by giants in clusters [J].
Bassino, LP ;
Muzzio, JC ;
Pérez, J .
CELESTIAL MECHANICS & DYNAMICAL ASTRONOMY, 1998, 72 (03) :157-168
[6]   RAPID ACCUMULATION OF ELASTIN AND COLLAGEN IN THE AORTAS OF SHEEP IN THE IMMEDIATE PERINATAL-PERIOD [J].
BENDECK, MP ;
LANGILLE, BL .
CIRCULATION RESEARCH, 1991, 69 (04) :1165-1169
[7]   Regulation of transglutaminases by nitric oxide [J].
Bernassola, F ;
Rossi, A ;
Melino, G .
MECHANISMS OF CELL DEATH: THE SECOND ANNUAL CONFERENCE OF THE CELL DEATH SOCIETY, 1999, 887 :83-91
[8]   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
[10]   EVALUATION OF EXTRACELLULAR-MATRIX TURNOVER - METHODS AND RESULTS FOR NORMAL HUMAN LUNG PARENCHYMAL ELASTIN [J].
CAMPBELL, E ;
PIERCE, J ;
ENDICOTT, S ;
SHAPIRO, S .
CHEST, 1991, 99 (03) :S49-S49