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- W4221043960 endingPage "1699" @default.
- W4221043960 startingPage "1686" @default.
- W4221043960 abstract "Blood vessels normally remain stable over the long term. However, in atherosclerosis, vascular cells leave the quiescent state and enter an activated state. Here, we investigated the factors that trigger the breakage of the quiescent state by screening growth factors and cytokines using a vascular smooth muscle cell (SMC) line and an endothelial cell (EC) line. Despite known functions of the tested factors, only basic fibroblast growth factor (bFGF) was identified as a potent trigger of quiescence breakage in SMCs, but not ECs. bFGF disrupted tight SMC‐monolayers and caused morphological changes, proliferation, and dedifferentiation. Human primary SMCs, but not ECs, also showed similar results. Aberrant SMC proliferation is a critical histological event in atherosclerosis. We, thus, provide further insights into the role of bFGF in vascular pathobiology." @default.
- W4221043960 created "2022-04-03" @default.
- W4221043960 creator A5012563387 @default.
- W4221043960 creator A5056911111 @default.
- W4221043960 date "2022-04-06" @default.
- W4221043960 modified "2023-10-01" @default.
- W4221043960 title "Basic fibroblast growth factor uniquely stimulates quiescent vascular smooth muscle cells and induces proliferation and dedifferentiation" @default.
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- W4221043960 doi "https://doi.org/10.1002/1873-3468.14345" @default.
- W4221043960 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35363891" @default.
- W4221043960 hasPublicationYear "2022" @default.
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