Evidence map›Paper›PMID 41263626›Full record

ArticleClinical genetics2026

Expanding the Genotype and Phenotype Diversity in a Chinese Cohort With TRPV4-Related Dysplasia.

Lina Dong, Kwan Chun Ho, Zhijia Tan, Yanni He, Yapeng Zhou, Shijie Yin, Lin Feng, Janus Siu Him Wong, Michael Kai Tsun To

Abstract read
In one paragraph

Article in Clinical genetics, 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. Article
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.

Lina DongDepartment of Orthopaedics and Traumatology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Kwan Chun HoDepartment of Orthopaedics and Traumatology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong.
Zhijia TanDepartment of Orthopaedics and Traumatology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Yanni HeDepartment of Orthopaedics and Traumatology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Yapeng ZhouDepartment of Orthopaedics and Traumatology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Shijie YinDepartment of Orthopaedics and Traumatology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Lin FengDepartment of Orthopaedics and Traumatology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
Janus Siu Him WongDepartment of Orthopaedics and Traumatology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.ORCID 0000-0003-1361-4733
Michael Kai Tsun ToDepartment of Orthopaedics and Traumatology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.

Funding

National Natural Science Foundation of China 82472392Sanming Project of Medicine in Shenzen Municipality SZSM202311022Shenzhen Clinical Research Center for Rare Diseases LCYSSQ20220823091402005Shenzhen-Hong Kong cooperation zone for technology and innovation HZQSWS-KCCYB-2024055Shenzhen Science and Technology Innovation Program JCYJ20230807113500001
6 · The paper itself

Abstract

Dominant mutations in the calcium permeable ion channel TRPV4 (transient receptor potential vanilloid 4) typically result in skeletal dysplasia or peripheral neuromuscular disease. However, the full spectrum of TRPV4-related phenotypes remains incompletely defined. This study systematically reviewed the clinical and genetic features of 10 Chinese patients harboring various TRPV4 variants. In the cohort, six patients were diagnosed with spondylometaphyseal dysplasia Kozlowski type (SMDK) and four patients with metatropic dysplasia (MD). The most common features involved spinal deformity (platyspondyly, kyphosis or scoliosis), and lower-limb malalignments (genu varum, genu valgum, or leg-length discrepancy). Two patients with MD had neurological deficits. The R594H and P799R substitutions were the most recurrent variants in our study. A novel variant (c.1628T>G, p.L543R) in the S2-S3 loop was identified. The study seeks to improve diagnostic precision by combining genetic and radiographic assessment, and highlights the importance of early spinal surveillance and multidisciplinary care to prevent neurological complications underlying TRPV4-mediated disorders.

Indexed as

DwarfismGenetic Predisposition to DiseaseOsteochondrodysplasiasTRPV Cation ChannelsAdolescentChildChild, PreschoolChinaCohort StudiesEast Asian PeopleFemaleGenetic Association StudiesGenotypeHumansInfantMaleTRPV4 protein, humanTRPV Cation Channelsgenotypephenotypeskeletal dysplasiaTRPV4‐Related dysplasia

Identifiers

PMID41263626
PMCPMC12958006

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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.