ArticleBiomedical reports2022
Cilostazol regulates the expressions of endothelin-1 and endothelial nitric oxide synthase via activation of the p38 MAPK signaling pathway in HUVECs.
Article in Biomedical reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- Research progress of platelets in neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- Direct simulation of hypertensive stress on endothelial cells: a streamlined model of in-vitro-hypertension.Frontiers in physiology · 2025Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
Cilostazol is a selective inhibitor of phosphodiesterase type III that inhibits platelet aggregation. The beneficial effects of cilostazol have been attributed not only to its antiplatelet functions but also to its actions on the endothelium. Whether cilostazol regulates endothelin-1 (ET-1) and endothelial nitric oxide synthase (eNOS) through mitogen-activated protein kinase (MAPK) remains undetermined. The aim of this study was to investigate the effects of cilostazol on ET-1 and eNOS expression in HUVECs, and to assess its relationship with MAPK activity. HUVECs were cultured
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