Evidence map›Paper›PMID 28799229›Full record

ArticleJournal of cellular and molecular medicine2018

Sitagliptin-mediated preservation of endothelial progenitor cell function via augmenting autophagy enhances ischaemic angiogenesis in diabetes.

Xiaozhen Dai, Jun Zeng, Xiaoqing Yan, Qian Lin, Kai Wang, Jing Chen, Feixia Shen, Xuemei Gu, Yuehui Wang, Jun Chen and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 63 citations in OpenAlex.

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  11. Exogenous HBioengineered · 2022
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  12. Sitagliptin attenuates endothelial dysfunction independent of its blood glucose controlling effect.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
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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

14 authors at 4 institutions in 2 countries.

Xiaozhen DaiChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, School of Nursing at the Wenzhou Medical University, Wenzhou, China.
Jun ZengPediatric Research Institute, Department of Pediatrics, University of Louisville School of Medicine, Louisville, USA.
Xiaoqing YanChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, School of Nursing at the Wenzhou Medical University, Wenzhou, China.
Qian LinPediatric Research Institute, Department of Pediatrics, University of Louisville School of Medicine, Louisville, USA.
Kai WangPediatric Research Institute, Department of Pediatrics, University of Louisville School of Medicine, Louisville, USA.
Jing ChenPediatric Research Institute, Department of Pediatrics, University of Louisville School of Medicine, Louisville, USA.
Feixia ShenDepartments of Pediatrics, Endocrinology and Metabolism, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Xuemei GuDepartments of Pediatrics, Endocrinology and Metabolism, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Yuehui WangDepartments of Geriatrics, the First Hospital of Jilin University, Changchun, China.
Jun ChenChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, School of Nursing at the Wenzhou Medical University, Wenzhou, China.
Kejian PanSchool of Biomedicine, Chengdu Medical College, Chengdu, China.
Lu CaiChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, School of Nursing at the Wenzhou Medical University, Wenzhou, China.
Kupper A WintergerstDepartment of Pediatrics, Division of Endocrinology, Wendy L. Novak Diabetes Care Center, University of Louisville, Louisville, KY, USA.
Yi TanChinese-American Research Institute for Diabetic Complications, School of Pharmaceutical Sciences, School of Nursing at the Wenzhou Medical University, Wenzhou, China.ORCID 0000-0002-9798-6237
University of Louisville · USWenzhou Medical University · CNChengdu Medical College · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, the dipeptidyl peptidase-4 (DPP-4) inhibitor sitagliptin, a major anti-hyperglycaemic agent, has received substantial attention as a therapeutic target for cardiovascular diseases via enhancing the number of circulating endothelial progenitor cells (EPCs). However, the direct effects of sitagliptin on EPC function remain elusive. In this study, we evaluated the proangiogenic effects of sitagliptin on a diabetic hind limb ischaemia (HLI) model in vivo and on EPC culture in vitro. Treatment of db/db mice with sitagliptin (Januvia) after HLI surgery efficiently enhanced ischaemic angiogenesis and blood perfusion, which was accompanied by significant increases in circulating EPC numbers. EPCs derived from the bone marrow of normal mice were treated with high glucose to mimic diabetic hyperglycaemia. We found that high glucose treatment induced EPC apoptosis and tube formation impairment, which were significantly prevented by sitagliptin pretreatment. A mechanistic study found that high glucose treatment of EPCs induced dramatic increases in oxidative stress and apoptosis; pretreatment of EPCs with sitagliptin significantly attenuated high glucose-induced apoptosis, tube formation impairment and oxidative stress. Furthermore, we found that sitagliptin restored the basal autophagy of EPCs that was impaired by high glucose via activating the AMP-activated protein kinase/unc-51-like autophagy activating kinase 1 signalling pathway, although an autophagy inhibitor abolished the protective effects of sitagliptin on EPCs. Altogether, the results indicate that sitagliptin-induced preservation of EPC angiogenic function results in an improvement of diabetic ischaemia angiogenesis and blood perfusion, which are most likely mediated by sitagliptin-induced prevention of EPC apoptosis via augmenting autophagy.

Indexed as

AutophagyNeovascularization, PhysiologicAMP-Activated Protein KinasesAnimalsAutophagy-Related Protein-1 HomologBone Marrow CellsCell SurvivalDiabetes Mellitus, Type 2Endothelial Progenitor CellsGlucoseHindlimbIschemiaMaleMicePerfusionReactive Oxygen SpeciesAMP-Activated Protein KinasesAutophagy-Related Protein-1 HomologGlucoseReactive Oxygen SpeciesSitagliptin PhosphateUlk1 protein, mouseangiogenesisautophagyendothelial progenitor cellshind limb ischaemiasitagliptin

Identifiers

PMID28799229
PMCPMC5742710
OpenAlexW2744978480

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.