Evidence map›Paper›PMID 30444033›Full record

ArticleJournal of cellular and molecular medicine2019

Vildagliptin improves high glucose-induced endothelial mitochondrial dysfunction via inhibiting mitochondrial fission.

Hengdao Liu, Hong Xiang, Shaoli Zhao, Haiqiang Sang, Fenghua Lv, Ruifang Chen, Zhihao Shu, Alex F Chen, Shuhua Chen, Hongwei Lu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 53 citations in OpenAlex.

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  18. DPP4 as a Potential Candidate in Cardiovascular Disease.Journal of inflammation research · 2022
    Review
  19. Frontiers in cell and developmental biology · 2022
    Article
  20. 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

10 authors at 3 institutions in 2 countries.

Hengdao LiuCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Hong XiangCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Shaoli ZhaoCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Haiqiang SangDepartment of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Fenghua LvDepartment of Cardiology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, China.
Ruifang ChenCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Zhihao ShuCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Alex F ChenCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Shuhua ChenCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.
Hongwei LuCenter for Experimental Medical Research, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China.ORCID 0000-0001-9589-5975
Central South University · CNFirst Affiliated Hospital of Xinxiang Medical University · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dipeptidyl peptidase 4 inhibitor vildagliptin (VLD), a widely used anti-diabetic drug, exerts favourable effects on vascular endothelium in diabetes. We determined for the first time the improving effects of VLD on mitochondrial dysfunction in diabetic mice and human umbilical vein endothelial cells (HUVECs) cultured under hyperglycaemic conditions, and further explored the mechanism behind the anti-diabetic activity. Mitochondrial ROS (mtROS) production was detected by fluorescent microscope and flow cytometry. Mitochondrial DNA damage and ATP synthesis were analysed by real time PCR and ATPlite assay, respectively. Mitochondrial network stained with MitoTracker Red to identify mitochondrial fragmentation was visualized under confocal microscopy. The expression levels of dynamin-related proteins (Drp1 and Fis1) were determined by immunoblotting. We found that VLD significantly reduced mtROS production and mitochondrial DNA damage, but enhanced ATP synthesis in endothelium under diabetic conditions. Moreover, VLD reduced the expression of Drp1 and Fis1, blocked Drp1 translocation into mitochondria, and blunted mitochondrial fragmentation induced by hyperglycaemia. As a result, mitochondrial dysfunction was alleviated and mitochondrial morphology was restored by VLD. Additionally, VLD promoted the phosphorylation of AMPK and its target acetyl-CoA carboxylase in the setting of high glucose, and AMPK activation led to a decreased expression and activation of Drp1. In conclusion, VLD improves endothelial mitochondrial dysfunction in diabetes, possibly through inhibiting Drp1-mediated mitochondrial fission in an AMPK-dependent manner.

Indexed as

Acetyl-CoA CarboxylaseAMP-Activated Protein KinasesAnimalsDiabetes Mellitus, ExperimentalDNA, MitochondrialDynaminsEndothelium, VascularGene Expression RegulationGlucoseHumansHuman Umbilical Vein Endothelial CellsHypoglycemic AgentsMaleMiceMice, Inbred C57BLMice, TransgenicAcetyl-CoA CarboxylaseAMP-Activated Protein KinasesDNA, MitochondrialDnm1l protein, mouseDynaminsGlucoseHypoglycemic AgentsMitochondrial ProteinsReactive Oxygen SpeciesVildagliptinAMPKDrp1mitochondrial dysfunctionmitochondrial fissionmitochondrial reactive oxygen speciesvildagliptin

Identifiers

PMID30444033
PMCPMC6349192
OpenAlexW2901021262

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.