Evidence map›Paper›PMID 28374486›Full record

ArticleJournal of cellular and molecular medicine2017

A Novel CXCR4 antagonist enhances angiogenesis via modifying the ischaemic tissue environment.

Xiaoqing Yan, Xiaozhen Dai, Luqing He, Xiao Ling, Minglong Shao, Chi Zhang, Yuehui Wang, Jian Xiao, Lu Cai, Xiaokun Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 12 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

11 authors at 3 institutions in 2 countries.

Xiaoqing YanChinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Chashan University-town, Wenzhou, Zhejiang, China.
Xiaozhen DaiPediatric Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY, USA.
Luqing HeChinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Chashan University-town, Wenzhou, Zhejiang, China.
Xiao LingChinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Chashan University-town, Wenzhou, Zhejiang, China.
Minglong ShaoChinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Chashan University-town, Wenzhou, Zhejiang, China.
Chi ZhangChinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Chashan University-town, Wenzhou, Zhejiang, China.
Yuehui WangDepartment of Geriatric Medicine, the first hospital of Jilin university, Changchun, Jilin, China.
Jian XiaoChinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Chashan University-town, Wenzhou, Zhejiang, China.
Lu CaiChinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Chashan University-town, Wenzhou, Zhejiang, China.
Xiaokun LiChinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Chashan University-town, Wenzhou, Zhejiang, China.
Yi TanChinese-American Research Institute for Diabetic Complications, Wenzhou Medical University, Chashan University-town, Wenzhou, Zhejiang, China.ORCID 0000-0002-9798-6237
Wenzhou Medical University · CNUniversity of Louisville · USJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial progenitor cells (EPCs) play a capital role in angiogenesis via directly participating in neo-vessel formation and secreting pro-angiogenic factors. Stromal cell-derived factor 1 (SDF-1) and its receptor CXCR4 play a critical role in the retention and quiescence of EPCs within its niche in the bone marrow. Disturbing the interaction between SDF-1 and CXCR4 is an effective strategy for EPC mobilization. We developed a novel CXCR4 antagonist P2G, a mutant protein of SDF-1β with high antagonistic activity against CXCR4 and high potency in enhancing ischaemic angiogenesis and blood perfusion. However, its direct effects on ischaemic tissue remain largely unknown. In this study, P2G was found to possess a robust capability to promote EPC infiltration and incorporation in neo-vessels, enhance the expression and function of pro-angiogenic factors, such as SDF-1, vascular endothelial growth factor and matrix metalloprotein-9, and activate cell signals involved in angiogenesis, such as proliferating cell nuclear antigen, protein kinase B (Akt), extracellular regulated protein kinases and mammalian target of rapamycin, in ischaemic tissue. Moreover, P2G can attenuate fibrotic remodelling to facilitate the recovery of ischaemic tissue. The capability of P2G in direct augmenting ischaemic environment for angiogenesis suggests that it is a potential candidate for the therapy of ischaemia diseases.

Indexed as

AnimalsBlood VesselsCell MovementChemokine CXCL12Endothelial Progenitor CellsIschemiaMaleMatrix Metalloproteinase 9Muscle, SkeletalPeptidesRats, Sprague-DawleyReceptors, CXCR4Signal TransductionVascular Endothelial Growth Factor AChemokine CXCL12Cxcr4 protein, ratMatrix Metalloproteinase 9PeptidesReceptors, CXCR4Vascular Endothelial Growth Factor AAMD3100angiogenesisendothelial progenitor cellsP2G

Identifiers

PMID28374486
PMCPMC5618675
OpenAlexW2605276630

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.