Cited by 261Osteoarthritis Treatment and MechanismsProteoglycans and glycosaminoglycans researchProtease and Inhibitor Mechanisms

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Nitric oxide and inflammatory mediators in the perpetuation of osteoarthritis

Abramson, Steven B., Attur, Mukundan, Amin, Ashok R., Clancy, Robert·2001·Current Rheumatology Reports

DOI 10.1007/s11926-001-0069-3

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Abstract

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. PGE(2) 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.

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Authors: Abramson, S. B., Attur, M., Amin, A. R., & Clancy, R.
Affiliations: NYU Langone Health (US)
ORCID: Abramson, Steven B.
Attur, Mukundan
Amin, Ashok R.
Clancy, Robert
Venue: Current Rheumatology Reports
Publisher: Springer Science and Business Media LLC
Published: 2001-12
Volume: 3
Issue: 6
Pages: 535-541
ISSN: 1523-3774 (ISSN-L)
1534-6307
DOI: 10.1007/s11926-001-0069-3
OpenAlex: W2081577257
Cited by: 261
References: 63
Citations by year: 2026: 3 · 2025: 3 · 2024: 7 · 2023: 6 · 2022: 10 · 2021: 9 · 2020: 18 · 2019: 15 · 2018: 14 · 2017: 13 · 2016: 15 · 2015: 10 · 2014: 12 · 2013: 13 · 2012: 12
FWCI: 1.17
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Current Rheumatology Reports (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
Keywords: osteoarthritis, nitric oxide, articular chondrocytes, inflammatory mediators, inducible nitric oxide synthase, cyclooxygenase-2, prostaglandin E2, interleukin-1, inflammatory cytokines, apoptosis, cartilage degeneration, extracellular matrix, integrins, biomechanical forces, autocrine and paracrine signaling
MeSH terms: Cartilage, Articular, Humans, Nitric Oxide, Osteoarthritis, Cytokines, Inflammation Mediators, Nitric Oxide Synthase, Nitric Oxide Synthase Type II

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Nitric oxide and inflammatory mediators in the perpetuation of osteoarthritis

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