ArticleInternational journal of molecular sciences2021
Cilostazol Induces eNOS and TM Expression via Activation with Sirtuin 1/Krüppel-like Factor 2 Pathway in Endothelial Cells.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- RNA sequencing-based profiling of differentially expressed microRNAs in endothelial cells from offspring of hypertensive pregnancies: a preliminary study.Frontiers in molecular biosciences · 2025Article
- From Microcirculation to Aging-Related Diseases: A Focus on Endothelial SIRT1.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Article
- Integrated analysis of the lncRNA-associated competing endogenous RNA network in salt sensitivity of blood pressure.Heliyon · 2023Article
- SIRT1 and thrombosis.Frontiers in molecular biosciences · 2023Review
- Trichostatin D as a Novel KLF2 Activator Attenuates TNFα-Induced Endothelial Inflammation.International journal of molecular sciences · 2022Article
- Effects of a Phosphodiesterase inhibitor on the Browning of Adipose Tissue in Mice.Biomedicines · 2022Article
- Generation of Functional Cardiomyocytes from Human Gastric Fibroblast-Derived Induced Pluripotent Stem Cells.Biomedicines · 2021Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Cilostazol was suggested to be beneficial to retard in-stent atherosclerosis and prevent stent thrombosis. However, the mechanisms responsible for the beneficial effects of cilostazol are not fully understood. In this study, we attempted to verify the mechanism of the antithrombotic effect of cilostazol. Human umbilical vein endothelial cells (HUVECs) were cultured with various concentrations of cilostazol to verify its impact on endothelial cells. KLF2, silent information regulator transcript-1 (SIRT1), endothelial nitric oxide synthase (eNOS), and endothelial thrombomodulin (TM) expression levels were examined. We found cilostazol significantly activated KLF2 expression and KLF2-related endothelial function, including eNOS activation, Nitric oxide (NO) production, and TM secretion. The activation was regulated by SIRT1, which was also stimulated by cilostazol. These findings suggest that cilostazol may be capable of an antithrombotic and vasculoprotective effect in endothelial cells.
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