Evidence map›Paper›PMID 32096219›Full record

ArticleJournal of cellular physiology2020

Oxidative stress-induced RAC autophagy can improve the HUVEC functions by releasing exosomes.

Linxin Zhu, Jiankun Zang, Bing Liu, Guocheng Yu, Lili Hao, Lian Liu, Jingxiang Zhong

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular physiology, 2020. 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
2.5field-weighted citation impact, top 10% 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, 49 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

7 authors at 2 institutions in 1 country.

Linxin ZhuDepartment of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Jiankun ZangDepartment of Neurology and Stroke Center, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Bing LiuDepartment of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Guocheng YuDepartment of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Lili HaoDepartment of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Lian LiuDepartment of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Jingxiang ZhongDepartment of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, China.ORCID 0000-0002-5774-7602
First Affiliated Hospital of Jinan University · CNRisun (China) · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retinal neovascularization (RNV) is a common pathological feature in many kinds of fundus oculi diseases. Sometimes RNV can even lead to severe vision loss. Oxidative injury is one of the main predisposing factors for RNV occurrence and development. The specific mechanism may be closely related to the special structural tissues of the retina. Retinal astrocytes (RACs) are mesenchymal cells located in the retinal neuroepithelial layer. RACs have an intimate anatomical relationship with microvascular endothelial cells. They have a variety of functions, but little is known about the mechanisms by which RACs regulate the function of endothelial cells. The molecules secreted by RACs, such as exosomes, have recently received a lot of attention and may provide potential clues to address the RAC-mediated modulation of endothelial cells. In this study, we aimed to preliminarily explore the mechanisms of how RAC exosomes generated under oxidative stress are involved in the regulation of endothelial function. Our results showed that the apoptosis and autophagy levels in RACs were positively correlated with the oxidative stress level, and the exosomes generated from RACs under normal and oxidative stress conditions had different effects on the proliferation and migration of endothelial cells. However, the effect of RACs on endothelial cell function could be markedly reversed by the autophagy inhibitor 3-methyladenine or the exosome inhibitor GW4869. Therefore, oxidative stress can lead to increased autophagy in RACs and can further promote RACs to regulate endothelial cell function by releasing exosomes.

Indexed as

ApoptosisAstrocytesAutophagyCell MovementCell ProliferationCells, CulturedEndothelial CellsExosomesHumansHuman Umbilical Vein Endothelial CellsMesenchymal Stem CellsOxidative StressRetinaRetinal Neovascularizationautophagyexosomeoxidative stressretinal astrocytestert-butyl hydroperoxide (tBHP)

Identifiers

PMID32096219
PMCPMC7496456
OpenAlexW3008857816

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.