Evidence map›Paper›PMID 39400871›Full record

ArticleScience China. Life sciences2025

RGS22 maintains the physiological function of ependymal cells to prevent hydrocephalus.

Xue Pang, Lin Gu, Qiu-Ying Han, Jia-Qing Xing, Ming Zhao, Shao-Yi Huang, Jun-Xi Yi, Jie Pan, Hao Hong, Wen Xue and 15 more

Abstract read
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In one paragraph

Article in Science China. Life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
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

25 authors.

Xue Pang *Nanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Lin Gu *Nanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Qiu-Ying HanNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Jia-Qing XingNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Ming ZhaoNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Shao-Yi HuangNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Jun-Xi YiNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Jie PanNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Hao HongNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Wen XueNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Xue-Qing ZhouNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Zhi-Hui SuNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Xin-Ran ZhangNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Li-Ming SunNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Shao-Zhen JiangNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Dan LuoNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Ling ChenNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Zheng-Jie WangNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Yu YuNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Tian XiaNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Xue-Min ZhangNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Ai-Ling LiNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Tao ZhouNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China.
Hong CaiNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China. hcai@xmail.ncba.ac.cn.
Tao LiNanhu Laboratory, National Center of Biomedical Analysis, Beijing, 100039, China. tli@ncba.ac.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ependymal cells line the wall of cerebral ventricles and ensure the unidirectional cerebrospinal fluid (CSF) flow by beating their motile cilia coordinately. The ependymal denudation or ciliary dysfunction causes hydrocephalus. Here, we report that the deficiency of regulator of G-protein signaling 22 (RGS22) results in severe congenital hydrocephalus in both mice and rats. Interestingly, RGS22 is specifically expressed in ependymal cells within the brain. Using conditional knock-out mice, we further demonstrate that the deletion of Rgs22 exclusively in nervous system is sufficient to induce hydrocephalus. Mechanistically, we show that Rgs22 deficiency leads to the ependymal denudation and impaired ciliogenesis. This phenomenon can be attributed to the excessive activation of lysophosphatidic acid receptor (LPAR) signaling under Rgs22

Indexed as

EpendymaHydrocephalusRGS ProteinsAnimalsCiliaMiceMice, Inbred C57BLMice, KnockoutRatsReceptors, Lysophosphatidic AcidSignal TransductionReceptors, Lysophosphatidic AcidRGS Proteinsependymal cellshydrocephalusRGS22

Identifiers

PMID39400871

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.