ArticleScientific reports2026
Clopidogrel bisulfate modulates metabolic activity and ERK-associated signaling in human endothelial progenitor cells under oxidative stress: an in vitro study.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Endothelial progenitor cells (EPCs) play a critical role in vascular repair and neovascularization by contributing to endothelial regeneration. While clopidogrel bisulfate is widely used as an antiplatelet agent, its direct cellular effects on EPC biology remain largely unexplored. This study aimed to determine whether clopidogrel bisulfate modulates human EPC proliferation, survival, and intracellular signaling in vitro. Human EPCs were isolated from peripheral blood mononuclear cells and characterized by Dil-ac-LDL uptake and CD34 immunostaining. Cells were treated with clopidogrel bisulfate (0, 5, or 10 µM) for 48 h. Proliferation, apoptosis, and cell viability were assessed using microscopy, Annexin V/PI flow cytometry, and CCK-8 assays. Western blotting was used to evaluate apoptosis-related proteins (Bax, Bcl-2) and signaling pathways (p-ERK). Clopidogrel bisulfate-treated EPCs maintained characteristic morphology and exhibited an apparent increase in cell density compared with untreated controls, without significant induction of apoptosis. CCK-8 assay revealed increased absorbance at later reaction time points, indicating enhanced cellular metabolic activity. In addition, under basal conditions, no consistent changes in the Bax/Bcl-2 ratio or ERK phosphorylation were observed. In contrast, under H
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