Evidence map›Paper›PMID 37185898›Full record

ArticleCell discovery2023

The asymmetrical ESR1 signaling in muscle progenitor cells determines the progression of adolescent idiopathic scoliosis.

Xiexiang Shao, Xin Fu, Jingfan Yang, Wenyuan Sui, Sheng Li, Wenjun Yang, Xingzuan Lin, Yuanyuan Zhang, Minzhi Jia, Huan Liu and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
12.4field-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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  3. ESR1 as a candidate gene for adolescent idiopathic scoliosis pathogenesis in North-West Indian population.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026
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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 4 institutions in 1 country.

Xiexiang Shao *Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xin Fu *Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jingfan Yang *Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wenyuan Sui *Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Sheng Li *Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wenjun Yang *Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xingzuan LinXinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuanyuan ZhangState Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai, China.
Minzhi JiaCentre Testing International Medical Laboratory (CTI-Medlab), Shanghai, China.
Huan LiuCentre Testing International Medical Laboratory (CTI-Medlab), Shanghai, China.
Wei LiuCentre Testing International Medical Laboratory (CTI-Medlab), Shanghai, China.
Lili HanCentre Testing International Medical Laboratory (CTI-Medlab), Shanghai, China.
Yang YuCentre Testing International Medical Laboratory (CTI-Medlab), Shanghai, China.
Yaolong DengXinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Tianyuan ZhangXinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Junlin YangXinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. yangjunlin@xinhuamed.com.cn.
Ping HuXinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. hup@sibcb.ac.cn.ORCID http://orcid.org/0000-0001-8832-1391
Shanghai Jiao Tong University · CNShanghai International Medical Center · CNChinese Academy of Sciences · CNXinHua Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82072519
6 · The paper itself

Abstract

Adolescent Idiopathic Scoliosis (AIS) is a common pediatric skeletal disease highly occurred in females. The pathogenesis of AIS has not been fully elucidated. Here, we reveal that ESR1 (Estrogen Receptor 1) expression declines in muscle stem/progenitor cells at the concave side of AIS patients. Furthermore, ESR1 is required for muscle stem/progenitor cell differentiation and disrupted ESR1 signaling leads to differentiation defects. The imbalance of ESR1 signaling in the para-spinal muscles induces scoliosis in mice, while reactivation of ESR1 signaling at the concave side by an FDA approved drug Raloxifene alleviates the curve progression. This work reveals that the asymmetric inactivation of ESR1 signaling is one of the causes of AIS. Reactivation of ESR1 signaling in para-spinal muscle by Raloxifene at the concave side could be a new strategy to treat AIS.

Identifiers

PMID37185898
PMCPMC10130095
OpenAlexW4366985527

What OpenQuestion holds

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LicenceCC BY
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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.