Evidence map›Paper›PMID 28963101›Full record

ArticleJournal of the American Heart Association2017

Chronic Psychological Stress Accelerates Vascular Senescence and Impairs Ischemia-Induced Neovascularization: The Role of Dipeptidyl Peptidase-4/Glucagon-Like Peptide-1-Adiponectin Axis.

Limei Piao, Guangxian Zhao, Enbo Zhu, Aiko Inoue, Rei Shibata, Yanna Lei, Lina Hu, Chenglin Yu, Guang Yang, Hongxian Wu and 6 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 66 citations in OpenAlex.

  1. Liraglutide Ameliorates Injury-Related Vascular Repair by Activating Autophagy Through Modulation of the PI3K-mTOR Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
  3. Increased Dipeptidyl Peptidase-4 Promotes Adipose Inflammation and Dysfunction in Mice Under Chronic Stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  4. Review
  5. Dipeptidyl peptidase-4 deficiency prevents chronic stress-induced cardiac remodeling and dysfunction in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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  10. Cathepsin K deficiency prevented stress-related thrombosis in a mouse FeClCellular and molecular life sciences : CMLS · 2024
    Article
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  20. Pre-delivery angiogenic factors and their association with peripartum perceived stress and pain in pre-eclampsia with severe features and normotensive pregnancies.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2022
    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

16 authors at 3 institutions in 3 countries.

Limei PiaoDepartment of Community Healthcare & Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Guangxian ZhaoCardiology and ICU, Yanbian University Hospital, Yanji, Jilin Province, China.
Enbo ZhuCardiology and ICU, Yanbian University Hospital, Yanji, Jilin Province, China.
Aiko InoueDepartment of Community Healthcare & Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Rei ShibataDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Yanna LeiDepartment of Community Healthcare & Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Lina HuDepartment of Community Healthcare & Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Chenglin YuDepartment of Community Healthcare & Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Guang YangDepartment of Community Healthcare & Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hongxian WuDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Wenhu XuDepartment of Community Healthcare & Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Kenji OkumuraDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Noriyuki OuchiDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Toyoaki MuroharaDepartment of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Masafumi KuzuyaDepartment of Community Healthcare & Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Xian Wu ChengDepartment of Community Healthcare & Geriatrics, Nagoya University Graduate School of Medicine, Nagoya, Japan chengxw0908@163.com xianwu@med.nagoya-u.ac.jp.
Nagoya University · JPYanbian University Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExposure to psychosocial stress is a risk factor for cardiovascular disease, including vascular aging and regeneration. Given that dipeptidyl peptidase-4 (DPP4) regulates several intracellular signaling pathways associated with the glucagon-like peptide-1 (GLP-1) metabolism, we investigated the role of DPP4/GLP-1 axis in vascular senescence and ischemia-induced neovascularization in mice under chronic stress, with a special focus on adiponectin -mediated peroxisome proliferator activated receptor-γ/its co-activator 1α (PGC-1α) activation. METHODS AND

resultsSeven-week-old mice subjected to restraint stress for 4 weeks underwent ischemic surgery and were kept under immobilization stress conditions. Mice that underwent ischemic surgery alone served as controls. We demonstrated that stress impaired the recovery of the ischemic/normal blood-flow ratio throughout the follow-up period and capillary formation. On postoperative day 4, stressed mice showed the following: increased levels of plasma and ischemic muscle DPP4 and decreased levels of GLP-1 and adiponectin in plasma and phospho-AMP-activated protein kinase α (p-AMPKα), vascular endothelial growth factor, peroxisome proliferator activated receptor-γ, PGC-1α, and Sirt1 proteins and insulin receptor 1 and glucose transporter 4 genes in the ischemic tissues, vessels, and/or adipose tissues and numbers of circulating endothelial CD31

conclusionsThese results indicate that the DPP4/GLP-1-adiponectin axis is a novel therapeutic target for the treatment of vascular aging and cardiovascular disease under chronic stress conditions.

Indexed as

Cellular SenescenceNeovascularization, PhysiologicAdiponectinAnimalsCells, CulturedChronic DiseaseDipeptidyl Peptidase 4Disease Models, AnimalEndothelial Progenitor CellsGlucagon-Like Peptide 1IschemiaMaleMice, Inbred C57BLPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR gammaProteolysisAdiponectinadiponectin receptor 1, mouseAdipoq protein, mouseAdipoq protein, ratDipeptidyl Peptidase 4Dpp4 protein, mouseDPP4 protein, ratGlucagon-Like Peptide 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPAR gammaPpargc1a protein, mouseReceptors, Adiponectinagingstressvascular biologyvascular diseasevascular endothelium

Identifiers

PMID28963101
PMCPMC5721852
OpenAlexW2759659176

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.