Evidence map›Paper›PMID 34584074›Full record

ArticleCell death & disease2021

Inhibition of nuclear receptor RORα attenuates cartilage damage in osteoarthritis by modulating IL-6/STAT3 pathway.

Tongzhou Liang, Taiqiu Chen, Jincheng Qiu, Wenjie Gao, Xianjian Qiu, Yuanxin Zhu, Xudong Wang, Yanbo Chen, Hang Zhou, Zhihuai Deng and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 53 citations in OpenAlex.

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  18. Bone-muscle crosstalk under physiological and pathological conditions.Cellular and molecular life sciences : CMLS · 2024
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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

17 authors at 1 institution in 1 country.

Tongzhou Liang *Department of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0000-0001-5920-5412
Taiqiu Chen *Department of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Jincheng Qiu *Department of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Wenjie Gao *Department of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Xianjian QiuDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Yuanxin ZhuDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Xudong WangDepartment of Orthopedics, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Yanbo ChenDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Hang ZhouDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Zhihuai DengDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Pengfei LiDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Caixia XuResearch Centre for Translational Medicine, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Yan PengDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Anjing LiangDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Peiqiang SuDepartment of Orthopedics, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Bo GaoDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China. gaob5@mail.sysu.edu.cn.ORCID 0000-0003-4578-0234
Dongsheng HuangDepartment of Orthopedics, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China. hdongsh@mail.sysu.edu.cn.ORCID 0000-0002-2824-300X
Sun Yat-sen University · CN

Funding

China Postdoctoral Science Foundation 2019TQ0377Guangdong Science and Technology Department (Science and Technology Department, Guangdong Province) 2019A030317003National Natural Science Foundation of China (National Science Foundation of China) 82072473Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2018A030313096Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2021A1515012619
6 · The paper itself

Abstract

Osteoarthritis (OA) is characterized by cartilage destruction, chronic inflammation, and local pain. Evidence showed that retinoic acid receptor-related orphan receptor-α (RORα) is crucial in cartilage development and OA pathogenesis. Here, we investigated the role and molecular mechanism of RORα, an important member of the nuclear receptor family, in regulating the development of OA pathologic features. Investigation into clinical cartilage specimens showed that RORα expression level is positively correlated with the severity of OA and cartilage damage. In an in vivo OA model induced by anterior crucial ligament transaction, intra-articular injection of si-Rora adenovirus reversed the cartilage damage. The expression of cartilage matrix components type II collagen and aggrecan were elevated upon RORα blockade. RNA-seq data suggested that the IL-6/STAT3 pathway is significantly downregulated, manifesting the reduced expression level of both IL-6 and phosphorylated STAT3. RORα exerted its effect on IL-6/STAT3 signaling in two different ways, including interaction with STAT3 and IL-6 promoter. Taken together, our findings indicated the pivotal role of the RORα/IL-6/STAT3 axis in OA progression and confirmed that RORα blockade improved the matrix catabolism in OA chondrocytes. These results may provide a potential treatment target in OA therapy.

Indexed as

Signal TransductionAgedAnimalsBase SequenceBenzamidesCartilage, ArticularChondrocytesDisease Models, AnimalDown-RegulationFemaleFluorocarbonsHumansInterleukin-6MaleMiceMice, Inbred C57BLBenzamidesFluorocarbonsInterleukin-6Nuclear Receptor Subfamily 1, Group F, Member 1RNA, MessengerSR 1078SR 3335STAT3 Transcription FactorSulfonamidesThiophenes

Identifiers

PMID34584074
PMCPMC8478978
OpenAlexW3202279394

What OpenQuestion holds

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Registered trials

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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.