Evidence map›Paper›PMID 29363056›Full record

ArticleMolecular and cellular biochemistry2018

Recombinant human maspin inhibits high glucose-induced oxidative stress and angiogenesis of human retinal microvascular endothelial cells via PI3K/AKT pathway.

Feng Qiu, Huijuan Tong, Yawen Wang, Jun Tao, Hailin Wang, Lei Chen

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Effect of Shuangdan Mingmu Capsule on Diabetic Retinopathy in Rats via Regulation of miRNAs.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022
    Article
  7. Article
  8. Article
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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

6 authors at 3 institutions in 1 country.

Feng QiuDepartment of Ophthalmology, Shenyang Fourth People's Hospital, 20 South Huanghe Avenue, Shenyang, 110031, People's Republic of China. qiu20042004@163.com.
Huijuan TongDepartment of Nursing, Shenyang Medical College, Shenyang, 110034, People's Republic of China.
Yawen WangDepartment of Ophthalmology, Shenyang Fourth People's Hospital, 20 South Huanghe Avenue, Shenyang, 110031, People's Republic of China.
Jun TaoDepartment of Ophthalmology, Shenyang Fourth People's Hospital, 20 South Huanghe Avenue, Shenyang, 110031, People's Republic of China.
Hailin WangDepartment of Ophthalmology, Shenyang Fourth People's Hospital, 20 South Huanghe Avenue, Shenyang, 110031, People's Republic of China.
Lei ChenDepartment of Ophthalmology, The First Affiliated Hospital of China Medical University, Shenyang, 110001, People's Republic of China.
Shenyang The Fourth Hospital of People · CNFirst Hospital of China Medical University · CNShenyang Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maspin is known as a tumor suppressor and a potent angiogenesis inhibitor, however, its effects on proliferative diabetic retinopathy (PDR) have not been fully elucidated. This study aimed at evaluating the effects of maspin on high glucose-induced oxidative stress and angiogenesis in human retinal microvascular endothelial cells (HRMECs). Herein, HRMECs were treated with 0.25, 0.5, or 1 µM recombinant human maspin in the presence of 30 mM glucose, and their proliferation, tube formation, and oxidative stress responses were further detected. Our results revealed that maspin inhibited the high glucose-induced proliferation, migration, and tube formation of HRMECs. Maspin also decreased reactive oxygen species, nitric oxide level, and increased glutathione S-transferase activity in HRMECs. Meanwhile, maspin reduced the mRNA and protein levels of hypoxia-inducible factor-1α and vascular endothelial growth factor in high glucose-stimulated cells in a dose-dependent manner. Additionally, the high glucose-induced elevation of phosphorylated phosphoinositide-3-kinase (p-PI3K) and phosphorylated AKT was also suppressed by maspin. In summary, our data suggest that maspin inhibits high glucose-induced proliferation, oxidative stress, and angiogenesis of HRMECs at least by modulating the PI3K/AKT pathway. Maspin may be a potential therapeutic agent for the prevention and treatment of PDR.

Indexed as

Diabetic RetinopathyEndothelial CellsGlucoseHumansNeovascularization, PhysiologicOxidative StressPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRecombinant ProteinsRetinal VesselsSerpinsSignal TransductionGlucosePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRecombinant ProteinsSERPIN-B5SerpinsAngiogenesisHuman retinal microvascular endothelial cellsMaspinPI3K/AKTProliferative diabetic retinopathy

Identifiers

PMID29363056
OpenAlexW2784507338

What OpenQuestion holds

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Read underepoch 390

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.