Evidence map›Paper›PMID 27316923›Full record

ArticleCardiovascular diabetology2016

Metformin improves the angiogenic functions of endothelial progenitor cells via activating AMPK/eNOS pathway in diabetic mice.

Jia-Wen Yu, Ya-Ping Deng, Xue Han, Guo-Fei Ren, Jian Cai, Guo-Jun Jiang

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
11.1field-weighted citation impact, top 1% 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

91 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

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  17. Oral Active Carbon Quantum Dots for Diabetes.Pharmaceuticals (Basel, Switzerland) · 2024
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31 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Jia-Wen YuDepartment of Pharmacy, Zhejiang Xiaoshan Hospital, Hangzhou, 311202, Zhejiang, China.
Ya-Ping DengDepartment of Pharmacy, Zhejiang Xiaoshan Hospital, Hangzhou, 311202, Zhejiang, China.
Xue HanDepartment of Pharmacy, Zhejiang Xiaoshan Hospital, Hangzhou, 311202, Zhejiang, China.
Guo-Fei RenDepartment of Pharmacy, Zhejiang Xiaoshan Hospital, Hangzhou, 311202, Zhejiang, China.
Jian CaiDepartment of Pharmacy, Zhejiang Xiaoshan Hospital, Hangzhou, 311202, Zhejiang, China.
Guo-Jun JiangDepartment of Pharmacy, Zhejiang Xiaoshan Hospital, Hangzhou, 311202, Zhejiang, China. jguojun999@163.com.
Zhejiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial dysfunction has been suggested as a possible causal link between hyperglycemia and microvascular complications in diabetes mellitus. The effect of metformin on endothelial progenitor cells (EPCs) is still unclear. This study was designed to test the hypothesis that metformin could accelerate wound healing by improving the impaired EPC functions in streptozotocin-induced diabetic mice.

methodsStreptozotocin (STZ, 60 mg/kg/d × 5 d, i.p.) was injected to induce type 1 diabetes in male C57BL/6 mice. Mice were treated with metformin (250 mg/kg/d, i.g.) for consecutive 14 days. Wound closure was evaluated by wound area and number of CD31 stained capillaries. Functions of bone marrow-endothelial progenitor cells (BM-EPCs) were assessed by tube formation and migration assays, and expression of AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) was determined by western blot analysis.

resultsMetformin accelerated wound closure and stimulated angiogenesis in diabetic mice. The number of circulating EPCs was increased significantly in metformin treated diabetic mice. Abilities of tube formation and migration of BM-EPCs were impaired in diabetic mice, which were improved by metformin. Expression of both phosphorylated-AMPK and phosphorylated-eNOS was significantly increased, and nitric oxide (NO) production was enhanced by metformin in BM-EPCs of diabetic mice. In vitro, metformin improved impaired BM-EPC functions, and increased phosphorylated-eNOS expression and NO production in cultured BM-EPCs caused by high glucose, which was prevented by the AMPK inhibitor compound C.

conclusionsOur results suggest that metformin could improve BM-EPC functions in STZ-induced diabetic mice, which was possibly dependent on the AMPK/eNOS pathway.

Indexed as

AMP-Activated Protein KinasesAnimalsCell MovementCells, CulturedDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Disease Models, AnimalEndothelial Progenitor CellsHyperglycemiaMaleMetforminMice, Inbred C57BLNitric Oxide Synthase Type IIISignal TransductionAMP-Activated Protein KinasesMetforminNitric Oxide Synthase Type IIINos3 protein, mouseAngiogenesisDiabetes mellitusEndothelial progenitor cells (EPCs)Metformin

Identifiers

PMID27316923
PMCPMC4912824
OpenAlexW2425790260

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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.