Evidence map›Paper›PMID 40995872›Full record

ReviewDevelopmental dynamics : an official publication of the American Association of Anatomists2026

Pathogenesis and potential therapeutic targets of trichorhinophalangeal syndrome; lessons obtained from animal studies.

Naoya Saeki, Rinna Kanai, Sayuri Tatsuta, Shinichi Kawaguchi, Masatsune Itoh, Shinsuke Ohba, Makoto Abe

Abstract readReview
In one paragraph

Review in Developmental dynamics : an official publication of the American Association of Anatomists, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Naoya SaekiDepartment of Tissue and Developmental Biology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Rinna KanaiDepartment of Tissue and Developmental Biology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Sayuri TatsutaDepartment of Tissue and Developmental Biology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Shinichi KawaguchiGraduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Masatsune ItohDepartment of Pediatrics, Kanazawa Medical University, Kahoku-gun, Ishikawa, Japan.
Shinsuke OhbaDepartment of Tissue and Developmental Biology, Osaka University Graduate School of Dentistry, Osaka, Japan.
Makoto AbeDepartment of Tissue and Developmental Biology, Osaka University Graduate School of Dentistry, Osaka, Japan.ORCID 0009-0005-2823-0881

Funding

Ministry of Education, Culture, Sports, Science and Technology 22K06295Ministry of Education, Culture, Sports, Science and Technology JP 16H06276Ministry of Education, Culture, Sports, Science and Technology JP 22H049Ministry of Education, Culture, Sports, Science and Technology KAKENHI 24K19841Takeda Science Foundation Research Grant 23K21494
6 · The paper itself

Abstract

Trichorhinophalangeal syndrome (TRPS) is a rare genetic disease inherited in an autosomal dominant manner. It occurs in 1 in 100,000 people globally and is caused by several types of mutations of the TRPS1 gene. Since the first human patient was reported in 1966, typical and atypical pathologies, disease courses, and treatment case presentations have been reported. TRPS is characterized by sparse slow-growing fine hair, a bulbous nose with tented nares, and brachydactyly with cone-shaped epiphyses on the hands and feet. Growth retardation and hip dysplasia are also frequently observed, suggesting that hair and skeletal phenotypes are the major pathologies of TRPS. Several animal models have been established and studied intensively to address this rare disease. However, comprehensive treatment strategies for TRPS have not been established. In this review, we summarize TRPS pathologies and the characteristics of TRPS1 as an atypical GATA-type transcription factor. We review rodent strains that have contributed to our understanding of the in vivo roles of Trps1 and discuss their validity as animal models of TRPS. We also summarize diseases that demonstrate pathologies similar to TRPS and findings in their animal models.

Indexed as

DNA-Binding ProteinsFingersHair DiseasesLanger-Giedion SyndromeNoseTranscription FactorsAnimalsDisease Models, AnimalGATA Transcription FactorsHumansMiceRepressor ProteinsDNA-Binding ProteinsGATA Transcription FactorsRepressor ProteinsTranscription FactorsTRPS1 protein, humandisease modelskeletal dysplasiatranscription factorTRPS1

Identifiers

PMID40995872
PMCPMC12994121

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.