Evidence map›Paper›PMID 27192932›Full record

ReviewNature reviews. Rheumatology2016

Ageing and the pathogenesis of osteoarthritis.

Richard F Loeser, John A Collins, Brian O Diekman

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Rheumatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 689 papers.

0numbers the graph read from it
0cells of the map it votes in
689citing papers in PubMed
50.0field-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

689 citing papers in PubMed, 1,223 citations in OpenAlex.

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629 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 2 institutions in 1 country.

Richard F LoeserThurston Arthritis Research Center, Division of Rheumatology, Allergy, and Immunology, 3300 Thurston Building, Campus Box 7280, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7280, USA.
John A CollinsThurston Arthritis Research Center, Division of Rheumatology, Allergy, and Immunology, 3300 Thurston Building, Campus Box 7280, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7280, USA.
Brian O DiekmanLineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, 450 West Drive, Campus Box 7295, Chapel Hill, North Carolina 27599-7295, USA.
University of North Carolina at Chapel Hill · USUNC Lineberger Comprehensive Cancer Center

Funding

Oxidative Stress and the Development of OsteoarthritisR01AG044034 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RICHARD F LOESER · 2012 to 2026
$5.7M
Defining the role of cellular senescence in osteoarthritisF32AG050399 · NIA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DIEKMAN, BRIAN O · 2015 to 2016
$108k
NIA NIH HHS F32 AG050399NIA NIH HHS R01 AG044034
6 · The paper itself

Abstract

Ageing-associated changes that affect articular tissues promote the development of osteoarthritis (OA). Although ageing and OA are closely linked, they are independent processes. Several potential mechanisms by which ageing contributes to OA have been elucidated. This Review focuses on the contributions of the following factors: age-related inflammation (also referred to as 'inflammaging'); cellular senescence (including the senescence-associated secretory phenotype (SASP)); mitochondrial dysfunction and oxidative stress; dysfunction in energy metabolism due to reduced activity of 5'-AMP-activated protein kinase (AMPK), which is associated with reduced autophagy; and alterations in cell signalling due to age-related changes in the extracellular matrix. These various processes contribute to the development of OA by promoting a proinflammatory, catabolic state accompanied by increased susceptibility to cell death that together lead to increased joint tissue destruction and defective repair of damaged matrix. The majority of studies to date have focused on articular cartilage, and it will be important to determine whether similar mechanisms occur in other joint tissues. Improved understanding of ageing-related mechanisms that promote OA could lead to the discovery of new targets for therapies that aim to slow or stop the progression of this chronic and disabling condition.

Indexed as

AgingAMP-Activated Protein KinasesAutophagyCartilage, ArticularCellular SenescenceChondrocytesDisease ProgressionHumansInflammationMitochondriaOsteoarthritisOxidative StressPhenotypeAMP-Activated Protein Kinases

Identifiers

PMID27192932
PMCPMC4938009
OpenAlexW2394631798

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.