Evidence map›Paper›PMID 38822888›Full record

ArticleCellular and molecular neurobiology2024

Astrocyte-Specific Inhibition of the Primary Cilium Suppresses C3 Expression in Reactive Astrocyte.

Nor Atiqah Muhamad, Kohei Masutani, Shota Furukawa, Shunsuke Yuri, Michinori Toriyama, Chuya Matsumoto, Seiya Itoh, Yuichiro Shinagawa, Ayako Isotani, Manami Toriyama and 1 more

Abstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Primary Cilia of Astrocytes in the Retina in Development and Disease.Investigative ophthalmology & visual science · 2026
    Article
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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

11 authors.

Nor Atiqah MuhamadDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan.
Kohei MasutaniDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan.
Shota FurukawaDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan.
Shunsuke YuriDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan.
Michinori ToriyamaDepartment of Biomedical Chemistry, School of Science and Technology, Kwansei Gakuin University, 1 Gakuenuegahara, Sanda, Hyogo, 669-1330, Japan.ORCID http://orcid.org/0000-0003-2551-4334
Chuya MatsumotoDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan.
Seiya ItohDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan.
Yuichiro ShinagawaDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan.
Ayako IsotaniDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan.ORCID http://orcid.org/0000-0002-4720-2318
Manami ToriyamaDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan. toriyama-m@bs.naist.jp.ORCID http://orcid.org/0000-0002-2754-293X
Hiroshi ItohDivision of Biological Science, Graduate School of Science and Technology, Nara Institute of Science and Technology, 8916-5, Takayama Cho, Ikoma, Nara, 630-0192, Japan. hitoh@bs.naist.jp.ORCID http://orcid.org/0000-0001-5793-0186

Funding

Japan Society for the Promotion of Science JP21K06382Japan Society for the Promotion of Science JP21K06837Japan Society for the Promotion of Science JP21K15087
6 · The paper itself

Abstract

C3-positive reactive astrocytes play a neurotoxic role in various neurodegenerative diseases. However, the mechanisms controlling C3-positive reactive astrocyte induction are largely unknown. We found that the length of the primary cilium, a cellular organelle that receives extracellular signals was increased in C3-positive reactive astrocytes, and the loss or shortening of primary cilium decreased the count of C3-positive reactive astrocytes. Pharmacological experiments suggested that Ca

Indexed as

AstrocytesCiliaMice, KnockoutAnimalsApoptosisComplement C3LipopolysaccharidesMiceMice, Inbred C57BLComplement C3LipopolysaccharidesAstrocytesConditional knockout mouseLPSPrimary ciliumTRPV4

Identifiers

PMID38822888
PMCPMC11144130

What OpenQuestion holds

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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.