Evidence map›Paper›PMID 41454937›Full record

ArticleCalcified tissue international2025

Clinical, Molecular Characteristics, and Genotype-Phenotype Relationships of Metaphyseal Chondrodysplasia Type Schmid.

Lingyang Meng, Jing Hu, Lei Sun, Qian Zhang, Ou Wang, Yan Jiang, Xiaoping Xing, Weibo Xia, Mei Li

Abstract readCase Reports
In one paragraph

Article in Calcified tissue international, 2025. 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.

Lingyang MengDepartment of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shuaifuyuan No. 1, Dongcheng District, Beijing, 100730, China.
Jing HuDepartment of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shuaifuyuan No. 1, Dongcheng District, Beijing, 100730, China.
Lei SunDepartment of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shuaifuyuan No. 1, Dongcheng District, Beijing, 100730, China.
Qian ZhangDepartment of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shuaifuyuan No. 1, Dongcheng District, Beijing, 100730, China.
Ou WangDepartment of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shuaifuyuan No. 1, Dongcheng District, Beijing, 100730, China.
Yan JiangDepartment of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shuaifuyuan No. 1, Dongcheng District, Beijing, 100730, China.
Xiaoping XingDepartment of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shuaifuyuan No. 1, Dongcheng District, Beijing, 100730, China.
Weibo XiaDepartment of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shuaifuyuan No. 1, Dongcheng District, Beijing, 100730, China.
Mei LiDepartment of Endocrinology, Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shuaifuyuan No. 1, Dongcheng District, Beijing, 100730, China. limeilzh@sina.com.ORCID http://orcid.org/0000-0001-7270-4902

Funding

CAMS Innovation Fund for Medical Sciences (CIFMS) 2021-I2M-1-051National High Level Hospital Clinical Research Funding 2022-PUMCH-B-014National Natural Science Foundation of China 82370894National Natural Science Foundation of China 82571026
6 · The paper itself

Abstract

Metaphyseal chondrodysplasia type Schmid (MCDS), a rare skeletal disorder caused by COL10A1 mutations, exhibits significant phenotypic heterogeneity, yet genotype-phenotype correlations remain poorly defined. We aim to determine the clinical and radiographic manifestation, mutational features, and genotype-phenotype relationships by characterization of 4 patients with MCDS and literature review. The four patients presented with short stature or waddling gait, flattened vertebrae, and irregular femoral epiphyses. We identified two novel COL10A1 variants (c.1925 T > A, c.1903C > G) and reported the first case harboring both a de novo nonsense (c.2001 T > G, p.Tyr667Ter) in the non-collagenous 1 (NC1) domain and a missense (c.1438A > T, p.Ile480Leu) in the helix domain. Genotype-phenotype analysis of 124 cases previously reported and 4 new cases revealed that NC1 domain mutations were associated with an earlier onset of MCDS than non-NC1 mutations (median 12 vs. 72 months, P = 0.0014). Patients carrying a missense mutation in COL10A1 showed significantly lower height Z-scores (- 3.62 ± 1.95 vs. - 1.99 ± 1.28, P = 0.013) at first and more metaphyseal irregularities in the distal radius/ulna than those with truncating mutations (P = 0.019). Structural modeling indicated that NC1 mutations may disrupt collagen X structure via electrostatic alterations or steric clashes. These findings expand the mutational spectrum of MCDS and establish that COL10A1 genotype correlates with severity of MCDS, which will help to identify patients with severe phenotypes through molecular testing and to develop effective treatment strategies for MCDS.

Indexed as

Collagen Type XOsteochondrodysplasiasOsteochondrosisChildChild, PreschoolFemaleGenetic Association StudiesGenotypeHumansInfantMaleMutationPhenotypeCOL10A1 protein, humanCollagen Type XCOL10A1Genotype–phenotype relationshipsMetaphyseal chondrodysplasia type SchmidType X collagen

Identifiers

PMID41454937
PMCPMC12743679

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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.