Nitric oxide and inflammatory mediators in the perpetuation of osteoarthritis

被引：229

作者：

Abramson S.B. ^{[1
]}

Attur M. ^{[1
]}

Amin A.R. ^{[1
]}

Clancy R. ^{[1
]}

机构：

[1] Departments of Medicine, Division of Rheumatology and the Department Pathology

[2] and the Department of Rheumatology and Medicine, Hospital for Joint Diseases, 301 East 17th Street, Room 1410, New York, 10003, NY

来源：

Current Rheumatology Reports | 2001年 / 3卷 / 6期

关键词：

Articular Cartilage; Articular Chondrocytes; Nitric Oxide; Proteoglycan Synthesis; Synovial Cell;

D O I：

10.1007/s11926-001-0069-3

中图分类号：

学科分类号：

摘要：

Articular chondrocyte production of nitric oxide (NO) and other inflammatory mediators, such as eicosanoids and cytokines, are increased in human osteoarthritis. The excessive production of nitric oxide inhibits matrix synthesis and promotes its degradation. Furthermore, by reacting with oxidants such as superoxide anion, nitric oxide promotes cellular injury and renders the chondrocyte susceptible to cytokine-induced apoptosis. PGE2 exerts anabolic and catabolic effects on chondrocytes, depending on the microenvironment and physiologic condition. The increased expression of inducible NOS (iNOS) and cyclo-oxygenase-2 (COX-2) in OA chondrocytes is largely due to the increased expression of pro-inflammatory cytokines, particularly IL-1, which act in an autocrine/paracrine fashion to perpetuate a catabolic state that leads to progressive destruction of articular cartilage. The initiating factors for the production of inflammatory mediators include altered biomechanical forces; their continued production may be augmented by an increase in extracellular matrix proteins acting through ligation of surface integrins. © 2001, Current Science Inc.

引用

页码：535 / 541

页数：6

共 61 条

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