Evidence map›Paper›PMID 35385310›Full record

ArticleScience advances2022

CXCL12/CXCR4-Rac1-mediated migration of osteogenic precursor cells contributes to pathological new bone formation in ankylosing spondylitis.

Haowen Cui, Zihao Li, Siwen Chen, Xiang Li, Dongying Chen, Jianru Wang, Zemin Li, Wenjun Hao, Fangling Zhong, Kuibo Zhang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.9field-weighted citation impact, top 4% of its field
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

12 citing papers in PubMed, 33 citations in OpenAlex.

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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

13 authors at 1 institution in 1 country.

Haowen CuiDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Zihao LiDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Siwen ChenDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.ORCID 0000-0003-2138-7737
Xiang LiDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Dongying ChenDepartment of Rheumatology and Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Jianru WangDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Zemin LiDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Wenjun HaoDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Fangling ZhongDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Kuibo ZhangDepartment of Spine Surgery, The Fifth Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Zhaomin ZhengDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Zhongping ZhanDepartment of Rheumatology and Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.
Hui LiuDepartment of Spine Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080 Guangdong, China.ORCID 0000-0003-0754-402X
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by inflammatory back pain and spinal ankylosis due to pathological new bone formation. Here, we identified CXCL12 as a critical contributor to pathological new bone formation through recruitment of osteogenic precursor cells (OPCs). CXCL12 was found highly expressed in the regions that would potentially develop pathological new bone. OPCs were recruited to the regions where CXCL12 was up-regulated. Inhibition of CXCL12/CXCR4 axis with AMD3100 or conditional knockout of CXCR4 attenuated OPCs migration and subsequent pathological new bone formation in animal models of AS. By contrast, a genetically engineered animal model with CXCL12 overexpression developed a joint ankylosis phenotype. Furthermore, Rac1 was found essential for OPCs migration and pathological new bone formation. These findings ravel the novel role of CXCL12 in AS and indicate a potential strategy for targeting the CXCL12/CXCR4-Rac1 axis to prevent progression of axial skeleton ankylosis.

Identifiers

PMID35385310
PMCPMC8986111
OpenAlexW4224222124

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

None linked

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.