ArticleExperimental and therapeutic medicine2014
Dihydroartemisinin inhibits vascular endothelial growth factor-induced endothelial cell migration by a p38 mitogen-activated protein kinase-independent pathway.
Article in Experimental and therapeutic medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- Dihydroartemisinin modulates the host proteome to suppress bovine viral diarrhea virus via mitochondrial and ER stress.Archives of microbiology · 2025Article
- Artemisinin and Its Derivatives: Promising Therapeutic Agents for Age-Related Macular Degeneration.Pharmaceuticals (Basel, Switzerland) · 2025Review
- MicroRNAs: Novel players in the diagnosis and treatment of cancer cachexia (Review).Experimental and therapeutic medicine · 2022Review
- Cadmium exposure enhances VE-cadherin expression in endothelial cells via suppression of ROCK signaling.Experimental and therapeutic medicine · 2022Article
- Dihydroartemisinin ameliorates chronic nonbacterial prostatitis and epithelial cellular inflammation by blocking the E2F7/HIF1α pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Dihydroartemisinin Inhibits Laser-Induced Choroidal Neovascularization in a Mouse Model of Neovascular AMD.Frontiers in pharmacology · 2022Article
- Dihydroartemisinin inhibits endothelial cell migration via the TGF-β1/ALK5/SMAD2 signaling pathway.Experimental and therapeutic medicine · 2021Article
- Dihydroartemisinin inhibits the expression of von Willebrand factor by downregulation of transcription factor ERG in endothelial cells.Fundamental & clinical pharmacology · 2021Article
- Artemisinin and artemisinin derivatives as anti-fibrotic therapeutics.Acta pharmaceutica Sinica. B · 2021Review
- Helicobacter Pylori Induces GATA3-Dependent Chitinase 3 Like 1 (CHI3L1) Upregulation and Contributes to Vascular Endothelial Injuries.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Dihydroartemisinin Induces Endothelial Cell Autophagy through Suppression of the Akt/mTOR Pathway.Journal of Cancer · 2019Article
- Dihydroartemisinin enhances VEGFR1 expression through up-regulation of ETS-1 transcription factor.Journal of Cancer · 2018Article
- Dihydroartemisinin transiently activates the JNK/SAPK signaling pathway in endothelial cells.Oncology letters · 2016Article
- Artemisinin and Its Derivatives as a Repurposing Anticancer Agent: What Else Do We Need to Do?Molecules (Basel, Switzerland) · 2016Review
- Dihydroartemisinin induces endothelial cell anoikis through the activation of the JNK signaling pathway.Oncology letters · 2016Article
- Updates on artemisinin: an insight to mode of actions and strategies for enhanced global production.Protoplasma · 2016Review
- Low-Dose Cadmium Upregulates VEGF Expression in Lung Adenocarcinoma Cells.International journal of environmental research and public health · 2015Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dihydroartemisinin (DHA), a semi-synthetic derivative of artemisinin, has been demonstrated to possess a strong antiangiogenic activity. However, the molecular mechanisms underlying this effect remain unclear. Endothelial cell (EC) migration is an essential component of angiogenesis, and the p38 mitogen-activated protein kinase (MAPK) signaling pathway plays a key role in the regulation of migration induced by vascular endothelial growth factor (VEGF). The aim of the present study was to investigate the effects of DHA on EC migration and the p38 MAPK signaling pathway. Human umbilical vein ECs (HUVECs) were treated with DHA and VEGF-induced migration was analyzed. The activation of p38 MAPK was detected by western blot analysis, and the migration assays were performed with a p38-specific inhibitor, SB203850. It was revealed that 20 μM DHA significantly reduced EC migration in the transwell migration assay, wound healing assay and electrical cell-substrate impedance sensing real-time analysis. However, DHA did not affect p38 MAPK phosphorylation or expression. In the absence or presence of SB203850, DHA induced a similar proportional reduction of EC migration in the three migration assays. Therefore, the present study demonstrated that DHA inhibits VEGF-induced EC migration via a p38 MAPK-independent pathway.
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