Evidence map›Paper›PMID 41836559›Full record

ArticleJournal of orthopaedic translation2026

Cyclin-dependent kinase 10 controls bone formation and is linked to human skeletal health.

Daiyang Yu, Tomoyuki Tanaka, Yuri Miyakoshi, Tsuyoshi Kato, Hiroki Ochi, Shingo Sato, Toshitaka Yoshii, Ali Al Kaissi, Philipp Kaldis, Hiroyuki Inose

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of orthopaedic translation, 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

10 authors.

Daiyang YuDepartment of Orthopaedics, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan.
Tomoyuki TanakaDepartment of Orthopedic Surgery, Dokkyo Medical University Saitama Medical Center, 2-1-50 Minamikoshigaya, Koshigaya, Saitama, 343-8555, Japan.
Yuri MiyakoshiDepartment of Orthopaedics, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan.
Tsuyoshi KatoDepartment of Orthopaedics, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan.
Hiroki OchiDepartment of Rehabilitation for Movement Functions, Research Institute, National Rehabilitation Center for Persons with Disabilities, 4-1 Namiki, Tokorozawa, Saitama, 359-8555, Japan.
Shingo SatoCenter for Innovative Cancer Treatment, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan.
Toshitaka YoshiiDepartment of Orthopaedics, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan.
Ali Al KaissiIlizarov National Medical Research Center for Traumatology and Orthopedics, 640014, Kurgan, Russia.
Philipp KaldisDepartment of Clinical Sciences, Lund University, Clinical Research Centre (CRC), Box 50332, SE-202 13, Malmö, Sweden.
Hiroyuki InoseDepartment of Orthopaedics, Institute of Science Tokyo, 1-5-45 Yushima, Bunkyo-Ku, Tokyo, 113-8519, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/objective: Bone remodeling is a critical process for skeletal health, and its dysregulation can lead to diseases like osteoporosis. While several Cyclin-Dependent Kinases (CDKs) are known to regulate bone metabolism, the function of CDK10 remains uncharacterized in this context. Human mutations in Methods: The Results: In vitro, both knockdown and overexpression of Conclusion: Our study establishes CDK10 as an essential regulator of osteoblast proliferation and bone formation The translational potential of this article: This research establishes Cyclin-Dependent Kinase 10 (CDK10) as a critical regulator of bone formation. Mouse studies demonstrate that osteoblast-specific Cdk10 deletion causes osteoporosis, mirroring osteopenia in humans with CDK10 mutations. These findings highlight CDK10 as a potential diagnostic marker and a novel therapeutic target for skeletal disorders characterized by impaired bone formation, such as osteoporosis.

Indexed as

Al Kaissi syndromeBglapBone formationCDK10Conditional knockoutOsteoblastOsteoporosis

Identifiers

PMID41836559
PMCPMC12988519

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.