Evidence map›Paper›PMID 29247173›Full record

ArticleNature communications2017

Estrogen-related receptor γ causes osteoarthritis by upregulating extracellular matrix-degrading enzymes.

Young-Ok Son, Seulki Park, Ji-Sun Kwak, Yoonkyung Won, Wan-Su Choi, Jinseol Rhee, Churl-Hong Chun, Je-Hwang Ryu, Don-Kyu Kim, Hueng-Sik Choi and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 77 citations in OpenAlex.

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  20. Oxymatrine Protects Chondrocytes against IL-1Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
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

11 authors at 3 institutions in 2 countries.

Young-Ok SonNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, 61005, Republic of Korea.ORCID http://orcid.org/0000-0003-0154-4061
Seulki ParkNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, 61005, Republic of Korea.
Ji-Sun KwakNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, 61005, Republic of Korea.
Yoonkyung WonNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, 61005, Republic of Korea.
Wan-Su ChoiNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, 61005, Republic of Korea.
Jinseol RheeNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, 61005, Republic of Korea.
Churl-Hong ChunDepartment of Orthopedic Surgery, Wonkwang University School of Medicine, Iksan, 54538, Republic of Korea.
Je-Hwang RyuResearch Center for Biomineralization Disorders, School of Dentistry, Chonnam National University, Gwangju, 61186, Republic of Korea.
Don-Kyu KimNational Creative Research Initiatives Center for Nuclear Receptor Signals and School of Biological Sciences and Technology, Chonnam National University, Gwangju, 61186, Republic of Korea.
Hueng-Sik ChoiNational Creative Research Initiatives Center for Nuclear Receptor Signals and School of Biological Sciences and Technology, Chonnam National University, Gwangju, 61186, Republic of Korea.
Jang-Soo ChunNational Creative Research Initiatives Center for Osteoarthritis Pathogenesis and School of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, 61005, Republic of Korea. jschun@gist.ac.kr.
Gwangju Institute of Science and Technology · KRChonnam National University · KRWonkwang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The estrogen-related receptor (ERR) family of orphan nuclear receptor is composed of ERRα, ERRβ, and ERRγ, which are known to regulate various isoform-specific functions under normal and pathophysiological conditions. Here, we investigate the involvement of ERRs in the pathogenesis of osteoarthritis (OA) in mice. Among ERR family members, ERRγ is markedly upregulated in cartilage from human OA patients and various mouse models of OA. Adenovirus-mediated overexpression of ERRγ in mouse knee joint or transgenic expression of ERRγ in cartilage leads to OA. ERRγ overexpression in chondrocytes directly upregulates matrix metalloproteinase (MMP)-3 and MMP13, which are known to play crucial roles in cartilage destruction in OA. In contrast, genetic ablation of Esrrg or shRNA-mediated downregulation of Esrrg in joint tissues abrogates experimental OA in mice. Our results collectively indicate that ERRγ is a novel catabolic regulator of OA pathogenesis.

Indexed as

AnimalsCells, CulturedChondrocytesGene Expression ProfilingHumansKnee JointMatrix Metalloproteinase 13Matrix Metalloproteinase 3Mice, Inbred C57BLMice, KnockoutMice, TransgenicOsteoarthritisReceptors, EstrogenRNA InterferenceUp-RegulationEsrrg protein, mouseMatrix Metalloproteinase 13Matrix Metalloproteinase 3Receptors, Estrogen

Identifiers

PMID29247173
PMCPMC5732273
OpenAlexW2772824541

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.