Evidence map›Paper›PMID 22788747›Full record

ArticleBritish journal of pharmacology2012

Dipeptidyl peptidase-4 inhibitor improves neovascularization by increasing circulating endothelial progenitor cells.

Chun-Yao Huang, Chun-Ming Shih, Nai-Wen Tsao, Yi-Wen Lin, Po-Hsun Huang, Shinn-Chih Wu, Ai-Wei Lee, Yung-Ta Kao, Nen-Chung Chang, Hironori Nakagami and 6 more

Abstract read
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In one paragraph

Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 84 citations in OpenAlex.

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  17. [Sitagliptin inhibits lipopolysaccharide-induced inflammatory response in human gingival fibroblasts by blocking nuclear factor-κB signaling pathway].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2021
    Article
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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

16 authors at 6 institutions in 2 countries.

Chun-Yao HuangGraduate Institute of Clinical Medicine, Taipei Medical University, Taipei, Taiwan.
Chun-Ming Shih
Nai-Wen Tsao
Yi-Wen Lin
Po-Hsun Huang
Shinn-Chih Wu
Ai-Wei Lee
Yung-Ta Kao
Nen-Chung Chang
Hironori Nakagami
Ryuichi Morishita
Keng-Liang Ou
Wen-Chi Hou
Cheng-Yen Lin
Kuo-Gi Shyu
Feng-Yen Lin
Taipei Medical University · TWTaipei Medical University Hospital · TWOsaka University · JPHungkuang University · TWNational Taiwan University of Science and Technology · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeCurrent methods used to treat critical limb ischaemia (CLI) are hampered by a lack of effective strategies, therefore, therapeutic vasculogenesis may open up a new field for the treatment of CLI. In this study we investigated the ability of the DPP-4 inhibitor, sitagliptin, originally used as a hypoglycaemic agent, to induce vasculogenesis in vivo. EXPERIMENTAL APPROACH: Sitagliptin were administered daily to C57CL/B6 mice and eGFP transgenic mouse bone marrow-transplanted ICR mice that had undergone hindlimb ischaemic surgery. Laser Doppler imaging and flow cytometry were used to evaluate the degree of neovasculogenesis and circulating levels of endothelial progenitor cells (EPCs) respectively. Cell surface markers of EPCs and endothelial NOS (eNOS) in vessels were studied. KEY

resultsSitagliptin elevated plasma glucagon-like peptide-1 (GLP-1) levels in mice subjected to ischaemia, decreased plasma dipeptidyl peptidase-4 (DPP-4) concentration, and augmented ischaemia-induced increases in stromal cell-derived factor-1 (SDF-1) in a dose-dependent manner. Blood flow in the ischaemic limb was significantly improved in mice treated with sitagliptin. Circulating levels of EPCs were also increased after sitagliptin treatment. Sitagliptin also enhanced the expression of CD 34 and eNOS in ischaemic muscle. In addition, sitagliptin promoted EPC mobilization and homing to ischaemic tissue in eGFP transgenic mouse bone marrow-transplanted ICR mice. CONCLUSION AND IMPLICATIONS: Circulating EPC levels and neovasculogenesis were augmented by the DPP-4 inhibitor, sitagliptin and this effect was dependent on an eNOS-related pathway in a mouse model of hindlimb ischaemia. The results indicate that oral administration of sitagliptin has therapeutic potential as an inducer of vasculogenesis.

Indexed as

AnimalsChemokine CXCL12Dipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsEndothelial CellsGlucagon-Like Peptide 1HindlimbIschemiaMaleMiceMice, Inbred ICRMice, TransgenicNeovascularization, PhysiologicNitric Oxide Synthase Type IIIPlatelet Endothelial Cell Adhesion Molecule-1PyrazinesChemokine CXCL12Dipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsGlucagon-Like Peptide 1Nitric Oxide Synthase Type IIINos3 protein, mousePlatelet Endothelial Cell Adhesion Molecule-1PyrazinesSitagliptin PhosphateTriazoles

Identifiers

PMID22788747
PMCPMC3514763
OpenAlexW1517096356

What OpenQuestion holds

Textmetadata
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.