Evidence map›Paper›PMID 31179340›Full record

ArticleJournal of diabetes research2019

To Explore the Pathogenesis of Vascular Lesion of Type 2 Diabetes Mellitus Based on the PI3K/Akt Signaling Pathway.

Jia-Rong Gao, Xiu-Juan Qin, Zhao-Hui Fang, Li-Shan, Li-Ping Han, Hui-Jiang, Ming-Fei Guo, Nan-Nan Jiang

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Jia-Rong GaoDepartment of Pharmacy, The First Affiliated Hospital of Anhui University of Chinese Medicine, 117 Meishan Road, Hefei, China.ORCID 0000-0002-8329-3106
Xiu-Juan QinDepartment of Pharmacy, The First Affiliated Hospital of Anhui University of Chinese Medicine, 117 Meishan Road, Hefei, China.
Zhao-Hui FangDepartment of Nephrology, The First Affiliated Hospital of Anhui University of Chinese Medicine, 117 Meishan Road, Hefei, China.
Li-ShanDepartment of Pharmacy, The First Affiliated Hospital of Anhui University of Chinese Medicine, 117 Meishan Road, Hefei, China.
Li-Ping HanDepartment of Pharmacy, The First Affiliated Hospital of Anhui University of Chinese Medicine, 117 Meishan Road, Hefei, China.
Hui-JiangDepartment of Pharmacy, The First Affiliated Hospital of Anhui University of Chinese Medicine, 117 Meishan Road, Hefei, China.
Ming-Fei GuoDepartment of Pharmacy, The First Affiliated Hospital of Anhui University of Chinese Medicine, 117 Meishan Road, Hefei, China.
Nan-Nan JiangDepartment of Pharmacy, The First Affiliated Hospital of Anhui University of Chinese Medicine, 117 Meishan Road, Hefei, China.
Anhui University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 2 diabetes mellitus (T2DM) has become a chronic disease, serious harm to human health. Complications of the blood pipe are the main cause of disability and death in diabetic patients, including vascular lesions that directly affects the prognosis of patients with diabetes and survival. This study was to determine the influence of high glucose and related mechanism of vascular lesion of type 2 diabetes mellitus pathogenesis.

methodsIn vivo aorta abdominalis of GK rats was observed with blood pressure, heart rate, hematoxylin and eosin (H&E), Masson, and Verhoeff staining. In vitro cells were cultured with 30 mM glucose for 24 h. RT-QPCR was used to detect the mRNA expression of endothelial markers PTEN, PI3K, Akt, and VEGF. Immunofluorescence staining was used to detect the expression of PTEN, PI3K, Akt, and VEGF. PI3K and Akt phosphorylation levels were detected by Western blot analysis.

resultsHeart rate, systolic blood pressure, diastolic blood pressure, and mean blood pressure in the GK control group were higher compared with the Wistar control group and no difference compared with the GK experimental model group. Fluorescence intensity of VEGF, Akt, and PI3K in the high-sugar stimulus group was stronger than the control group; PTEN in the high-sugar stimulus group was weakening than the control group. VEGF, Akt, and PI3K mRNA in the high-sugar stimulus group were higher than the control group; protein expressions of VEGF, Akt, and PI3K in the high-sugar stimulus group were higher than the control group. PTEN mRNA in the high-sugar stimulus group was lower than the control group. Protein expression of PTEN in the high-sugar stimulus group was lower than the control group.

conclusionsAngiogenesis is an important pathogenesis of T2DM vascular disease, and PTEN plays a negative regulatory role in the development of new blood vessels and can inhibit the PI3K/Akt signaling pathway.

Indexed as

Signal TransductionAnimalsAorta, AbdominalBlood GlucoseBlood PressureChronic DiseaseDiabetes Mellitus, Type 2GlycosylationHeart RateHumansHuman Umbilical Vein Endothelial CellsMaleNeovascularization, PathologicNG-Nitroarginine Methyl EsterPhosphatidylinositol 3-KinasesPhosphorylationBlood GlucoseNG-Nitroarginine Methyl EsterPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Messenger

Identifiers

PMID31179340
PMCPMC6501128
OpenAlexW2940236804

What OpenQuestion holds

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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.