Evidence map›Paper›PMID 40937144›Full record

ArticleFrontiers in cell and developmental biology2025

Slit2 inhibits SRC-PI3K signaling pathway, regulates osteoclast differentiation of macrophages and reduces bone resorption.

Qing Ge, Yaokun Zou, Huizhi Deng, Zhe Yang, Linhu Ge, Jieying Huang, Jianqiang Cai, Liping Wang

Abstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 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

8 authors.

Qing Ge *Department of Oral Implantology, School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction and Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yaokun Zou *Department of Oral Implantology, School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction and Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, Guangdong, China.
Huizhi Deng *Department of Oral Implantology, School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction and Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, Guangdong, China.
Zhe YangDepartment of Oral Implantology, School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction and Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, Guangdong, China.
Linhu GeDepartment of Oral Implantology, School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction and Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, Guangdong, China.
Jieying HuangDepartment of Oral Implantology, School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction and Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, Guangdong, China.
Jianqiang CaiDepartment of Oral Implantology, Suzhou Stomatological Hospital, Suzhou, China.
Liping WangDepartment of Oral Implantology, School and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction and Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis is a metabolic disorder characterized by increased bone resorption and decreased bone formation. As a well-characterized axon guidance molecule, Slit2 contributes to central nervous system regulation by modulating intracellular signaling cascades and is expressed in multiple tissues, including the nervous system and the kidneys. However, limited research has explored the role of Slit2 in bone metabolism, and its precise regulatory mechanisms remain unclear. In this study, we established an aging-induced osteoporosis model using wild-type (WT) and Slit2-transgenic (Slit2-Tg) mice, as well as an estrogen-deficient ovariectomy-induced osteoporosis model. Our findings demonstrate that Slit2 attenuates bone loss and suppresses osteoclast differentiation under osteoporotic conditions.

Indexed as

osteoclastsosteoporosisPI3K/AKT signalingSlit2Src

Identifiers

PMID40937144
PMCPMC12421006

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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.