Evidence map›Paper›PMID 22859926›Full record

ArticleTherapeutic advances in musculoskeletal disease2012

Chondrogenesis, chondrocyte differentiation, and articular cartilage metabolism in health and osteoarthritis.

Mary B Goldring

Abstract read
In one paragraph

Article in Therapeutic advances in musculoskeletal disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed, 1 pooled it
15.3field-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

203 citing papers in PubMed, 1 synthesis or guideline pooled it, 432 citations in OpenAlex.

  1. Pooled it
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  3. Preoperative high-intensity strength training improves postural control after TKA: randomized-controlled trial.Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA · 2019
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143 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

1 author at 1 institution in 1 country.

Mary B GoldringHospital for Special Surgery, Caspary Research Building, 5th Floor, 535 East 70th Street, New York, NY 10021, USA.
Hospital for Special Surgery · US

Funding

Defining Common Molecular Parameters For Onset and Progression of OsteoarthritisRC4AR060546 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI GOLDRING, MARY B, LI, YEFU · 2010 to 2010
$4.1M
Role of ESE1 Regulation of Type II Collagen in CartilageR01AG022021 · NIA · HOSPITAL FOR SPECIAL SURGERY · PI GOLDRING, MARY B · 2002 to 2014
$3.4M
ESE 1 a novel transcriptional regulator of cartilage remodelingR56AG022021 · NIA · HOSPITAL FOR SPECIAL SURGERY · PI GOLDRING, MARY B · 2009 to 2009
$438k
Epigenetic Regulation of MMP-13R21AR054887 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI GOLDRING, MARY B · 2007 to 2008
$355k
NIAMS NIH HHS R21 AR054887NIAMS NIH HHS RC4 AR060546NIA NIH HHS R01 AG022021NIA NIH HHS R56 AG022021
6 · The paper itself

Abstract

Chondrogenesis occurs as a result of mesenchymal cell condensation and chondroprogenitor cell differentiation. Following chondrogenesis, the chondrocytes remain as resting cells to form the articular cartilage or undergo proliferation, terminal differentiation to chondrocyte hypertrophy, and apoptosis in a process termed endochondral ossification, whereby the hypertrophic cartilage is replaced by bone. Human adult articular cartilage is a complex tissue of matrix proteins that varies from superficial to deep layers and from loaded to unloaded zones. A major challenge to efforts to repair cartilage by stem cell-based and other tissue-engineering strategies is the inability of the resident chondrocytes to lay down a new matrix with the same properties as it had when it was formed during development. Thus, understanding and comparing the mechanisms of cartilage remodeling during development, osteoarthritis (OA), and aging may lead to more effective strategies for preventing cartilage damage and promoting repair. The pivotal proteinase that marks OA progression is matrix metalloproteinase 13 (MMP-13), the major type II collagen-degrading collagenase, which is regulated by both stress and inflammatory signals. We and other investigators have found that there are common mediators of these processes in human OA cartilage. We also observe temporal and spatial expression of these mediators in early through late stages of OA in mouse models and are analyzing the consequences of knockout or transgenic overexpression of critical genes. Since the chondrocytes in adult human cartilage are normally quiescent and maintain the matrix in a low turnover state, understanding how they undergo phenotypic modulation and promote matrix destruction and abnormal repair in OA may to lead to identification of critical targets for therapy to block cartilage damage and promote effective cartilage repair.

Indexed as

articular cartilagechondrogenesisinflammationmouse modelsosteoarthritis

Identifiers

PMID22859926
PMCPMC3403254
OpenAlexW2111222524

What OpenQuestion holds

Textmetadata
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.