Cartilage biology in osteoarthritis-lessons from developmental biology

被引：196

作者：

Pitsillides, Andrew A. ^{[1
]}

Beier, Frank ^{[2
]}

机构：

[1] Univ London, Royal Vet Coll, Dept Vet Basic Sci, London NW1 OTU, England

[2] Univ Western Ontario, Schulich Sch Med & Dent, Dept Physiol & Pharmacol, London, ON N6A 5C1, Canada

来源：

NATURE REVIEWS RHEUMATOLOGY | 2011年 / 7卷 / 11期

基金：

英国生物技术与生命科学研究理事会; 加拿大健康研究院;

关键词：

HUMAN ARTICULAR-CARTILAGE; CHONDROCYTE HYPERTROPHIC DIFFERENTIATION; DEVELOPING APPENDICULAR SKELETON; ENDOCHONDRAL BONE-DEVELOPMENT; UDP-GLUCOSE DEHYDROGENASE; SYNOVIAL JOINT CAVITIES; TGF-BETA-SUPERFAMILY; AGE-RELATED-CHANGES; MEK-ERK PATHWAY; GENE-EXPRESSION;

D O I：

10.1038/nrrheum.2011.129

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The cellular and molecular mechanisms responsible for the initiation and progression of osteoarthritis (OA), and in particular cartilage degeneration in OA, are not completely understood. Increasing evidence implicates developmental processes in OA etiology and pathogenesis. Herein, we review this evidence. We first examine subtle changes in cartilage development and the specification and formation of joints, which predispose to OA development, and second, we review the switch from an articular to a hypertrophic chondrocyte phenotype that is thought to be part of the OA pathological process ultimately resulting in cartilage degeneration. The latest studies are summarized and we discuss the concepts emerging from these findings in cartilage biology, in the light of our understanding of the developmental processes involved.

引用

页码：654 / 663

页数：10

共 125 条

[1]

Aigner T, 1999, ARTHRITIS RHEUM, V42, P1443, DOI 10.1002/1529-0131(199907)42:7<1443::AID-ANR18>3.0.CO

[2]

2-A

[3] Osteo-chondroprogenitor cells are derived from Sox9 expressing precursors [J].

Akiyama, H ;

Kim, JE ;

Nakashima, K ;

Balmes, G ;

Iwai, N ;

Deng, JM ;

Zhang, ZP ;

Martin, JF ;

Behringer, RR ;

Nakamura, T ;

de Crombrugghe, B .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (41) :14665-14670

[4] Global analyses of gene expression in early experimental osteoarthritis [J].

Appleton, C. T. G. ;

Pitelka, V. ;

Henry, J. ;

Beier, F. .

ARTHRITIS AND RHEUMATISM, 2007, 56 (06) :1854-1868

[5] Forced mobilization accelerates pathogenesis: characterization of a preclinical surgical model of osteoarthritis [J].

Appleton, C. Thomas G. ;

McErlain, David D. ;

Pitelka, Vasek ;

Schwartz, Neil ;

Bernier, Suzanne M. ;

Henry, James L. ;

Holdsworth, David W. ;

Beier, Frank .

ARTHRITIS RESEARCH & THERAPY, 2007, 9 (01)

[6] Lack of HIF-2α in limb bud mesenchyme causes a modest and transient delay of endochondral bone development [J].

Araldi, Elisa ;

Khatri, Richa ;

Giaccia, Amato J. ;

Simon, M. Celeste ;

Schipani, Ernestina .

NATURE MEDICINE, 2011, 17 (01) :25-26

[7] SKELETAL DEVELOPMENT AND OSTEOARTHRITIS [J].

ARCHER, CW .

ANNALS OF THE RHEUMATIC DISEASES, 1994, 53 (10) :624-630

[8] Relationship between joint shape and the development of osteoarthritis [J].

Baker-LePain, Julie C. ;

Lane, Nancy E. .

CURRENT OPINION IN RHEUMATOLOGY, 2010, 22 (05) :538-543

[9]

Ballock R. Tracy, 2003, Birth Defects Research, V69, P123, DOI 10.1002/bdrc.10014

[10] Selective activation of the MEK-ERK pathway is regulated by mechanical stimuli in forming joints and promotes pericellular matrix formation [J].

Bastow, ER ;

Lamb, KJ ;

Lewthwaite, JC ;

Osborne, AC ;

Kavanagh, E ;

Wheeler-Jones, CPD ;

Pitsillides, AA .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (12) :11749-11758

← 1 2 3 4 5 6 7 8 9 10 →