Factor VII-activating protease deficiency promotes neointima formation by enhancing leukocyte accumulation.
J. Thromb. Haemost.2016 Oct;14(10):2058-2067. doi:10.1111/jth.13417. Epub 2016 Sep 07
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摘要
mice. This was due to an increased activity of the chemokine (C-C motif) ligand 2 (CCL2). SUMMARY:monocytes but not in the vessel wall. There was no difference in the expression of platelet-derived growth factor (PDGF-BB). Conclusions FSAP deficiency causes an increase in CCL2 expression and CCL2-mediated infiltration of leukocytes into the injured vessel, thereby promoting SMC proliferation and migration by the activation of leukocyte-derived gelatinases. These results provide a possible explanation for the observed association of the loss-of-function MI-SNP with vascular proliferative diseases.
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基因功能
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原始数据
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文献解读
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