Most recent developments in strategies to reduce the progression of structural changes in osteoarthritis: today and tomorrow

被引:54
作者
Pelletier, Jean-Pierre [1 ]
Martel-Pelletier, Johanne [1 ]
Raynauld, Jean-Pierre [1 ]
机构
[1] Univ Montreal Hosp Ctr, Osteoarthrit Res Unit, Notre Dame Hosp, Montreal, PQ, Canada
关键词
D O I
10.1186/ar1932
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Osteoarthritis (OA), the most common of all arthritic conditions, is a social and financial burden to all nations. The most recent research has significantly advanced our understanding of the cause of OA and risk factors associated with it. These findings have provided useful information that has helped in the daily management of patients with OA. Some preventative measures and a number of therapeutic agents and drugs are available, which may help to reduce the progression of OA in certain patients. Moreover, the most recent progress in research has significantly enhanced our knowledge of the factors involved in the development of the disease and of the mechanisms responsible for its progression. This has allowed identification of several new therapeutic targets in a number of pathophysiological pathways. Consequently, the field is opening up to a new era in which drugs and agents that can specifically block important mechanisms responsible for the structural changes that occur in OA can be brought into development and eventually into clinical trials.
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页数:14
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共 115 条
[1]   Cloning and characterization of ADAMTS11, an aggrecanase from the ADAMTS family [J].
Abbaszade, I ;
Liu, RQ ;
Yang, F ;
Rosenfeld, SA ;
Ross, OH ;
Link, JR ;
Ellis, DM ;
Tortorella, MD ;
Pratta, MA ;
Hollis, JM ;
Wynn, R ;
Duke, JL ;
George, HJ ;
Hillman, MC ;
Murphy, K ;
Wiswall, BH ;
Copeland, RA ;
Decicco, CP ;
Bruckner, R ;
Nagase, H ;
Itoh, Y ;
Newton, RC ;
Magolda, RL ;
Trzaskos, JM ;
Hollis, GF ;
Arner, EC ;
Burn, TC .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (33) :23443-23450
[2]   Phenyl N-tert-butylnitrone down-regulates interleukin-1β-stimulated matrix metalloproteinase-13 gene expression in human chondrocytes:: Suppression of c-jun NH2-terminal kinase, p38-mitogen-activated protein kinase and activating protein-1 [J].
Ahmed, S ;
Rahman, A ;
Hasnain, A ;
Goldberg, VM ;
Haqqi, TM .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2003, 305 (03) :981-988
[3]  
Aigner T, 2001, ARTHRITIS RHEUM-US, V44, P2777, DOI 10.1002/1529-0131(200112)44:12<2777::AID-ART465>3.0.CO
[4]  
2-H
[5]   Functional genomics of osteoarthritis [J].
Aigner, T ;
Bartnik, E ;
Zien, A ;
Zimmer, R .
PHARMACOGENOMICS, 2002, 3 (05) :635-650
[6]   Functional genomic analysis of type-II IL-1β decoy receptor:: Potential for gene therapy in human arthritis and inflammation [J].
Attur, MG ;
Dave, MN ;
Leung, MY ;
Cipolletta, C ;
Meseck, M ;
Woo, SLC ;
Amin, AR .
JOURNAL OF IMMUNOLOGY, 2002, 168 (04) :2001-2010
[7]   Reversal of autocrine and paracrine effects of interleukin 1 (IL-1) in human arthritis by type IIIL-1 decoy receptor - Potential for pharmacological intervention [J].
Attur, MG ;
Dave, M ;
Cipolletta, C ;
Kang, P ;
Goldring, MB ;
Patel, IR ;
Abramson, SB ;
Amin, AR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (51) :40307-40315
[8]  
Badger AM, 1996, J PHARMACOL EXP THER, V279, P1453
[9]  
Baker KR, 2001, J RHEUMATOL, V28, P1655
[10]   Genetic aspects of osteoarthritis [J].
Bateman, JF .
SEMINARS IN ARTHRITIS AND RHEUMATISM, 2005, 34 (06) :15-18