Evidence map›Paper›PMID 30176344›Full record

ReviewFree radical biology & medicine2019

Reactive oxygen species, aging and articular cartilage homeostasis.

Jesalyn A Bolduc, John A Collins, Richard F Loeser

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 363 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
363citing papers in PubMed, 4 pooled it
27.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

363 citing papers in PubMed, 4 syntheses or guidelines pooled it, 612 citations in OpenAlex.

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303 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Jesalyn A BolducDivision of Rheumatology, Allergy, and Immunology, University of North Carolina, Chapel Hill, NC, USA; Thurston Arthritis Research Center, University of North Carolina, Chapel Hill, NC, USA.
John A CollinsDivision of Rheumatology, Allergy, and Immunology, University of North Carolina, Chapel Hill, NC, USA; Thurston Arthritis Research Center, University of North Carolina, Chapel Hill, NC, USA.
Richard F LoeserDivision of Rheumatology, Allergy, and Immunology, University of North Carolina, Chapel Hill, NC, USA; Thurston Arthritis Research Center, University of North Carolina, Chapel Hill, NC, USA. Electronic address: richard_loeser@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Oxidative Stress and the Development of OsteoarthritisR01AG044034 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RICHARD F LOESER · 2012 to 2026
$5.7M
Integrin Function in CartilageR37AR049003 · NIAMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LOESER, RICHARD F · 2012 to 2021
$4.1M
Integrin Function in CartilageR01AR049003 · NIAMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LOESER, RICHARD F · 2002 to 2011
$2.8M
NIAMS NIH HHS R01 AR049003NIAMS NIH HHS R37 AR049003NIA NIH HHS R01 AG044034
6 · The paper itself

Abstract

Chondrocytes are responsible for the maintenance of the articular cartilage. A loss of homeostasis in cartilage contributes to the development of osteoarthritis (OA) when the synthetic capacity of chondrocytes is overwhelmed by processes that promote matrix degradation. There is evidence for an age-related imbalance in reactive oxygen species (ROS) production relative to the anti-oxidant capacity of chondrocytes that plays a role in cartilage degradation as well as chondrocyte cell death. The ROS produced by chondrocytes that have received the most attention include superoxide, hydrogen peroxide, the reactive nitrogen species nitric oxide, and the nitric oxide derived product peroxynitrite. Excess levels of these ROS not only cause oxidative-damage but, perhaps more importantly, cause a disruption in cell signaling pathways that are redox-regulated, including Akt and MAP kinase signaling. Age-related mitochondrial dysfunction and reduced activity of the mitochondrial superoxide dismutase (SOD2) are associated with an increase in mitochondrial-derived ROS and are in part responsible for the increase in chondrocyte ROS with age. Peroxiredoxins (Prxs) are a key family of peroxidases responsible for removal of H

Indexed as

AgingAnimalsCartilage, ArticularChondrocytesHomeostasisHumansMiceMitochondriaOsteoarthritisOxidative StressReactive Oxygen SpeciesSignal TransductionReactive Oxygen SpeciesAgingCartilageCell signalingChondrocytesOsteoarthritisReactive oxygen species

Identifiers

PMID30176344
PMCPMC6342625
OpenAlexW2889101189

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.