Evidence map›Paper›PMID 23611999›Full record

ArticleInvestigative ophthalmology & visual science2013

The artemisinin derivative artesunate inhibits corneal neovascularization by inducing ROS-dependent apoptosis in vascular endothelial cells.

Rui Cheng, Cen Li, Chaoyang Li, Ling Wei, Lei Li, Yang Zhang, Yachao Yao, Xiaoqiong Gu, Weibin Cai, Zhonghan Yang and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2013. 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
2.2field-weighted citation impact, top 12% 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, 55 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

13 authors at 5 institutions in 2 countries.

Rui ChengDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Cen Li
Chaoyang Li
Ling Wei
Lei Li
Yang Zhang
Yachao Yao
Xiaoqiong Gu
Weibin Cai
Zhonghan Yang
Jianxing Ma
Xia Yang
Guoquan Gao
Sun Yat-sen University · CNDepartment of Education of Guangdong Province · CNGuangdong Provincial People's Hospital · CNGuangzhou Medical University · CNUniversity of Oklahoma Health Sciences Center · US

Funding

Project 5 VEGF Signaling in PhotoreceptorsP20GM104934 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI LE, YUN ZHENG · 2012 to 2016
$10.8M
The wnt signaling pathway in choroidal neovascularizationR01EY018659 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI MA, JIAN-XING · 2009 to 2019
$3.7M
NEI NIH HHS R01 EY018659NIGMS NIH HHS P20 GM104934
6 · The paper itself

Abstract

purposeWithout therapeutic intervention, corneal neovascularization rapidly compromises visual acuity, and is a leading cause of blindness. Artesunate was reported to inhibit angiogenesis in tumors, although, the effects of artesunate on nontumor angiogenesis have not been investigated. This study was designed to investigate the effect of artesunate on corneal neovascularization and delineate its underlying mechanism of action.

methodsRats with alkali-burned corneas were treated with artesunate for 11 days. Corneal neovascularization was evaluated by measuring the length and area of corneal vasculature in the rats. Apoptotic cells were stained with AnnexinV and propidine iodide (PI), and measured with flow cytometry analysis. Apoptosis-related and p38 mitogen-activated protein kinases (p38MAPK) signaling were evaluated by Western blot analysis.

resultsArtesunate significantly inhibited corneal neovascularization and inflammation via specifically inducing apoptosis of vascular endothelial cells. In vascular endothelial cells, artesunate increased the Bax/Bcl-2 ratio, reduced mitochondrial membrane potential, stimulated release of cytochrome C, and cleavage of caspase 9 and 3, suggesting that the mitochondrial apoptotic pathway was involved. Artesunate activated p38MAPK, and specific p38MAPK inhibitors suppressed artesunate-induced apoptosis in endothelial cells. Reactive oxygen species (ROS) levels were increased by artesunate. N-acetyl-L-cysteine blocked p38MAPK activation and protected endothelial cells from artesunate-induced apoptosis. Ferrous salt increased ROS levels and elevated the cytotoxic effect of artesunate on endothelial cells, while the iron chelating agent deferoxamine decreased ROS levels and artesunate-induced apoptosis. Artesunate had no effect on expression of Fas, Fas Ligand, or caspase 8 cleavage.

conclusionsThese results suggest that artesunate induces apoptosis of endothelial cells via an iron/ROS-dependent p38MAPK-mitochondrial pathway.

Indexed as

Angiogenesis InhibitorsAnimalsAnnexin A5AntimalarialsApoptosisArtemisininsArtesunatebcl-2-Associated X ProteinBlotting, WesternBurns, ChemicalCorneal NeovascularizationDisease Models, AnimalEndothelial CellsEye BurnsFemaleFlow CytometryAngiogenesis InhibitorsAnnexin A5AntimalarialsArtemisininsArtesunateBax protein, ratbcl-2-Associated X Proteinp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesSodium Hydroxideapoptosisartemisinincorneal neovascularizationfree radicals

Identifiers

PMID23611999
PMCPMC5963000
OpenAlexW2054497342

What OpenQuestion holds

Textmetadata
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.