Evidence map›Paper›PMID 41769865›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

ZMAT1 Promotes Osteoclastogenesis Through TRIM46 Mediated YAP1 Degradation and Inhibits Osteoblastogenesis.

Xinyu Chang, Yijin Hou, Likun Cui, Huiqi Yu, Rong Liu, Junhao Sui, Zhong Zheng, Lu Liu, Jie Chen, Mengchen Chen and 4 more

Abstract read
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Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

14 authors.

Xinyu ChangDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Yijin HouDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Likun CuiNational Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai, China.
Huiqi YuDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Rong LiuDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Junhao SuiDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Zhong ZhengDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Lu LiuDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Jie ChenNational Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai, China.
Mengchen ChenDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Chen DingDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Shuogui XuDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.
Sheng XuNational Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai, China.
Hao ZhangDepartment of Traumatic Orthopedics, Changhai Hospital, Second Military Medical University, Shanghai, China.ORCID https://orcid.org/0000-0002-6347-2764

Funding

National Natural Science Foundation of China 81702666Shanghai Municipal Health Commission Smart Healthcare Project 2025ZHYL042Shanghai Science and Technology Innovation Action Plan 22S319004001
6 · The paper itself

Abstract

Osteoclasts and osteoblasts play critical roles in bone remodeling, and their dysregulation leads to pathological bone loss. However, the precise mechanisms underlying the regulation of differentiation remain unclear. This study investigated the role of the transcriptional regulator Zinc Finger Matrin-Type 1 (Zmat1) in both osteoclastogenesis and osteoblastogenesis. Zmat1 deficiency resulted in decreased osteoclast activity, and bone resorption. Mechanistically, ZMAT1 was significantly upregulated during osteoclast differentiation and acted as a transcriptional repressor of the E3 ubiquitin ligase TRIM46, which regulates YAP1 degradation via K48-linked ubiquitination. Furthermore, Zmat1 deficiency enhanced osteoblast activity and bone formation. These findings highlight a novel ZMAT1/TRIM46/YAP1 axis, providing new insights into the transcriptional regulation of both osteoclast and osteoblast differentiation, and present potential therapeutic targets for osteoporosis.

Indexed as

Adaptor Proteins, Signal TransducingOsteoblastsOsteoclastsOsteogenesisRNA-Binding ProteinsTranscription FactorsTripartite Motif ProteinsUbiquitin-Protein LigasesAnimalsCell DifferentiationHumansMiceYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingRNA-Binding ProteinsTranscription FactorsTripartite Motif ProteinsUbiquitin-Protein LigasesYap1 protein, mouseYAP-Signaling Proteinstranscription factorTRIM46ubiquitinationYAP1Zmat1

Identifiers

PMID41769865
PMCPMC13170258

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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.