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

Nitric oxide and inflammatory mediators in the perpetuation of osteoarthritis

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

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.

Integrity signals

Registry

Crossref · 10.1007/s11926-001-0069-3

Cites

61 of 61 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Articular cartilage of patients with osteoarthritis shows features of senescence, including increased nitric oxide and pro-inflammatory cytokines, p16, activated DNA damage response, ROS secretion and SA-β-Gal activity.

    “Articular cartilage of patients with OA shows features of senescence, including increased expression of nitric oxide, pro-inflammatory cytokines, particularly IL-1β [8]; p16 [9]; activated DNA damage response; ROS secretion and SA-β-Gal activity [10].”

Cites

Flagged first, then by citations

2 of the 63 references couldn’t be matched to a known paper.

Cited by

Sorted by citations

Authors
Abramson, S. B., Attur, M., Amin, A. R., & Clancy, R.
Affiliations
NYU Langone Health (US)
Venue
Current Rheumatology Reports
Published
2001-12
Volume
3
Issue
6
Pages
535-541
ISSN
  • 1523-3774 (ISSN-L)
  • 1534-6307
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
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review