Evidence map›Paper›PMID 39514089›Full record

ArticleJournal of bone and mineral metabolism2025

Meclozine and growth hormone ameliorate bone length and quality in experimental models of achondroplasia.

Kenta Sawamura, Masaki Matsushita, Ryusaku Esaki, Kenichi Mishima, Yasunari Kamiya, Kinji Ohno, Hiroshi Kitoh, Shiro Imagama

Abstract read
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In one paragraph

Article in Journal of bone and mineral metabolism, 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

8 authors.

Kenta SawamuraDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, Aichi, 466-8550, Japan.
Masaki MatsushitaDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, Aichi, 466-8550, Japan. matsushita.masaki.a7@f.mail.nagoya-u.ac.jp.ORCID http://orcid.org/0000-0003-4540-1556
Ryusaku EsakiDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, Aichi, 466-8550, Japan.
Kenichi MishimaDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, Aichi, 466-8550, Japan.
Yasunari KamiyaDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, Aichi, 466-8550, Japan.
Kinji OhnoDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Nagoya University Graduate School of Medicine, Nagoya, Aichi, 466-8550, Japan.
Hiroshi KitohDepartment of Orthopaedic Surgery, Aichi Children's Health and Medical Center, Obu, Aichi, 474-8017, Japan.
Shiro ImagamaDepartment of Orthopaedic Surgery, Nagoya University Graduate School of Medicine, 65 Tsurumai-Cho, Showa-Ku, Nagoya, Aichi, 466-8550, Japan.

Funding

Japan Agency for Medical Research and Development 24ek0109513h0004Japan Society for the Promotion of Science 19K09646Japan Society for the Promotion of Science 22K09398
6 · The paper itself

Abstract

introductionAchondroplasia (ACH) is a common skeletal dysplasia associated with short-limbed short stature caused by gain-of-function mutations in the fibroblast growth factor receptor 3 (FGFR3) gene. Meclozine was found to inhibit FGFR3 signaling using a drug repositioning strategy. In some countries, growth hormone (GH) has been employed to ameliorate short stature in children with ACH. This study aims to investigate the effects of meclozine and GH on bone growth and quality using an experimental model of ACH. MATERIALS AND

methodsMeclozine (2 mg/kg/day) and/or GH (0.35 mg/kg/day) were administered to a mouse model of ACH from the age of 7 to 56 days. Body length and body weight of each mouse were measured during these treatments. At the end of treatments, these mice were subjected to micro-computed tomography scans to measure the lengths of long bones and bone mineral density (BMD). The width of the growth plate was quantified by histological analysis.

resultsThe body and bone length of transgenic mice significantly increased after treatment with meclozine and GH, although there was no additive effect of the combination therapy on promoting bone growth. In contrast, BMD was additively increased by the combination therapy. The width of the growth plate in transgenic mice was significantly increased by both treatments, although the hypertrophic zone was enlarged by meclozine but not by GH.

conclusionMeclozine or GH may be an option for treating children with ACH to ameliorate bone length and quality, but the additive effect would be limited.

Indexed as

AchondroplasiaBone and BonesGrowth HormoneAnimalsBone DensityBone DevelopmentDisease Models, AnimalMaleMiceMice, TransgenicX-Ray MicrotomographyGrowth HormoneAchondroplasiaBone growthFibroblast growth factor receptor 3Growth hormoneMeclozine

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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.