Evidence map›Paper›PMID 40594392›Full record

ArticleScientific reports2025

Dusp1 in osteolytic diseases-mechanisms and therapeutic potential.

Boyu Liu, Ming Lei, Baicheng Wan, Yanbing Feng, Yilin Teng, Deshuang Xi, Shou Chen, Gaofeng Zeng, Shaohui Zong

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 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

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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

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.

Boyu Liu *Department of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, Guangxi, China.
Ming Lei *Department of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, Guangxi, China.
Baicheng WanDepartment of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, Guangxi, China.
Yanbing FengDepartment of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, Guangxi, China.
Yilin TengDepartment of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, Guangxi, China.
Deshuang XiDepartment of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, Guangxi, China.
Shou ChenDepartment of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, Guangxi, China.
Gaofeng ZengDepartment of Nutrition and Food Hygiene, College of Public Hygiene of Guangxi Medical University, No. 22, Shuangyong Road, Nanning, 530021, Guangxi, China. zenggaofeng@gxmu.edu.cn.
Shaohui ZongDepartment of Spine Osteopathia, The First Affiliated Hospital of Guangxi Medical University, Guangxi Medical University, No. 6, Shuangyong Road, Nanning, 530021, Guangxi, China. zongshaohui@gxmu.edu.cn.

Funding

Guangxi Medical High-level Key Talents Training "139" Program (2020)15Natural Science Foundation of Guangxi Zhuang Autonomous Region 2024GXNSFDA010035
6 · The paper itself

Abstract

Osteolytic diseases are a significant and escalating global public health issue, driven by the acceleration of population aging and the rising incidence of degenerative, metabolic, and neoplastic diseases. The primary therapeutic strategy for osteolytic diseases is to suppress the bone resorption activity of osteoclasts. Dusp1 is a member of the serine/threonine inducible nuclear phosphatase family and has significant anti-inflammatory effects. In this study, Dusp1 overexpression was induced via lentiviral transfection. We found that Dusp1 antagonized RANKL stimulation, mediated the MAPK signaling pathway, and downregulated the key downstream transcription factors c-FOS and NFATc1, thereby reducing the expression of osteoclast-specific genes. Furthermore, Dusp1 reduced the number and activity of osteoclasts both in vivo and in vitro, leading to a diminished bone resorption function. In addition, the results of animal experiments demonstrated that Dusp1 protected mice from LPS-induced skull osteolysis. Overall, our study reveals that Dusp1 suppresses osteoclast formation and activity by downregulating the MAPK/c-FOS/NFATc1 signaling pathway. These findings suggest the potential of Dusp1 to protect against osteolytic diseases.

Indexed as

Dual Specificity Phosphatase 1OsteolysisAnimalsBone ResorptionHumansLipopolysaccharidesMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLNFATC Transcription FactorsOsteoclastsProto-Oncogene Proteins c-fosRANK LigandRAW 264.7 CellsSignal TransductionDual Specificity Phosphatase 1DUSP1 protein, humanDusp1 protein, mouseLipopolysaccharidesNFATC Transcription FactorsProto-Oncogene Proteins c-fosRANK LigandDusp1LentivirusMAPKOsteoclastOsteolysisOverexpression

Identifiers

PMID40594392
PMCPMC12218375

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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.