Evidence map›Paper›PMID 41748604›Full record

ArticleNature communications2026

Excess FGFR3 signaling in achondroplasia disrupts turnover of resting zone chondrocytes via CREB signaling.

Nanao Horike, Seiya Oura, Saeko Koyamatsu, Noriko Tanaka, Yuki Iimori, Kaori Fujita, Takahiro Nemoto, Masahito Ikawa, Noriyuki Tsumaki

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Nanao HorikeDepartment of Tissue Biochemistry, Graduate School of Medicine, The University of Osaka, Suita-shi, Japan.
Seiya OuraDepartment of Experimental Genome Research, Research Institute for Microbial Diseases, The University of Osaka, Suita-shi, Japan.ORCID 0000-0002-7606-732X
Saeko KoyamatsuDepartment of Tissue Biochemistry, Graduate School of Medicine, The University of Osaka, Suita-shi, Japan.
Noriko TanakaDepartment of Tissue Biochemistry, Graduate School of Medicine, The University of Osaka, Suita-shi, Japan.
Yuki IimoriInstitute for Advanced Biosciences, Keio University, Tsuruoka-shi, Japan.
Kaori FujitaDepartment of Life Science, Graduate School of Engineering Science, Akita University, Akita-shi, Japan.
Takahiro NemotoPremium Research Institute for Human Metaverse Medicine (WPI-PRIMe), The University of Osaka, Suita-shi, Japan.ORCID 0000-0003-2981-4035
Masahito IkawaDepartment of Experimental Genome Research, Research Institute for Microbial Diseases, The University of Osaka, Suita-shi, Japan.ORCID 0000-0001-9859-6217
Noriyuki TsumakiDepartment of Tissue Biochemistry, Graduate School of Medicine, The University of Osaka, Suita-shi, Japan. tsumaki.noriyuki.med@osaka-u.ac.jp.ORCID 0000-0002-0520-3654

Funding

Japan Agency for Medical Research and Development (AMED) JP23bm1223014Japan Agency for Medical Research and Development (AMED) JP23ym0126127Japan Agency for Medical Research and Development (AMED) JP25bm1223026Kansai Startup Academia Coalition
6 · The paper itself

Abstract

Achondroplasia, associated with gain-of-function mutations in FGFR3, causes growth plate cartilage dysfunction, resulting in short-limb dwarfism. However, its precise molecular and cellular mechanisms remain unclear. To address this, we aimed to generate knock-in mice (Fgfr3

Indexed as

AchondroplasiaChondrocytesCyclic AMP Response Element-Binding ProteinReceptor, Fibroblast Growth Factor, Type 3AnimalsGene Knock-In TechniquesGrowth PlateMiceMutationSignal TransductionCyclic AMP Response Element-Binding ProteinFgfr3 protein, mouseReceptor, Fibroblast Growth Factor, Type 3

Identifiers

PMID41748604
PMCPMC12946275

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.