Factors controlling airway smooth muscle proliferation in asthma

被引:18
作者
Stewart, AG [1 ]
Bonacci, JV [1 ]
Quan, L [1 ]
机构
[1] Univ Melbourne, Dept Pharmacol, Melbourne, Vic 3010, Australia
基金
英国医学研究理事会;
关键词
D O I
10.1007/s11882-004-0055-8
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Airway smooth muscle proliferation has been the focus of considerable attention, as it is a quantitatively important component of the airway wall remodeling response in asthma and has been suggested as a sulable target for the development of novel anti-asthma agents. Such agents are considered likely to reduce airway hyperresponsiveness and, consequently, airway obstruction, resulting in fewer symptoms and exacerbations. Identifying suitable drug targets has proved an elusive goal, as no dominant molecular mechanism for remodeling has emerged. Moreover, recent findings raise some doubt as to whether smooth muscle proliferation per se is the explanation of the increase in smooth muscle cell number in asthma, with alternative explanations including the proposal that cells migrate either from the interstitial compartment or from a circulating precursor stem cell population. Therefore, drug targeting of migration responses should be considered as an alternative approach to regulating the smooth muscle component of airway wall remodeling.
引用
收藏
页码:109 / 115
页数:7
相关论文
共 58 条
[1]   IFN-γ inhibits human airway smooth muscle cell proliferation by modulating the E2F-1/Rb pathway [J].
Amrani, Y ;
Tliba, O ;
Choubey, D ;
Huang, CD ;
Krymskaya, VP ;
Eszterhas, A ;
Lazaar, AL ;
Panettieri, RA .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2003, 284 (06) :L1063-L1071
[2]   Mechanisms underlying TNF-alpha effects on agonist-mediated calcium homeostasis in human airway smooth muscle cells [J].
Amrani, Y ;
Krymskaya, V ;
Maki, C ;
Panettieri, RA .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1997, 273 (05) :L1020-L1028
[3]   Airway structural alterations selectively associated with severe asthma [J].
Benayoun, L ;
Druilhe, A ;
Dombret, MC ;
Aubier, M ;
Pretolani, M .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2003, 167 (10) :1360-1368
[4]   Collagen-induced resistance to glucocorticoid anti-mitogenic actions: a potential explanation of smooth muscle hyperplasia in the asthmatic remodelled airway [J].
Bonacci, JV ;
Harris, T ;
Wilson, JW ;
Stewart, AG .
BRITISH JOURNAL OF PHARMACOLOGY, 2003, 138 (07) :1203-1206
[5]   Asymptomatic airway hyperresponsiveness - A curiosity or an opportunity to prevent asthma? [J].
Boulet, LP .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2003, 167 (03) :371-378
[6]   Mast-cell infiltration of airway smooth muscle in asthma [J].
Brightling, CE ;
Bradding, P ;
Symon, FA ;
Holgate, ST ;
Wardlaw, AJ ;
Pavord, ID .
NEW ENGLAND JOURNAL OF MEDICINE, 2002, 346 (22) :1699-1705
[7]   HEPARAN SULFATE-DEGRADING ENZYMES INDUCE MODULATION OF SMOOTH-MUSCLE PHENOTYPE [J].
CAMPBELL, JH ;
RENNICK, RE ;
KALEVITCH, SG ;
CAMPBELL, GR .
EXPERIMENTAL CELL RESEARCH, 1992, 200 (01) :156-167
[8]   Collagen deposition in large airways may not differentiate severe asthma from milder forms of the disease [J].
Chu, HW ;
Halliday, JL ;
Martin, RJ ;
Leung, DYM ;
Szefler, SJ ;
Wenzel, SE .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1998, 158 (06) :1936-1944
[9]  
Dashtaki R, 1998, J PHARMACOL EXP THER, V285, P876
[10]   CD38-cyclic ADP-ribose-mediated Ca2+ signaling contributes to airway smooth muscle hyperresponsiveness [J].
Deshpande, DA ;
Walseth, TF ;
Panettieri, RA ;
Kannan, MS .
FASEB JOURNAL, 2003, 17 (01) :452-+