PTX3型
内皮功能障碍
炎症
基质金属蛋白酶
内皮干细胞
肿瘤坏死因子α
发病机制
癌症研究
内皮
一氧化氮
医学
细胞生物学
免疫学
生物
内科学
生物化学
体外
作者
Alexandru Zlibut,Ioana Corina Bocșan,Lucia Agoşton-Coldea
出处
期刊:Advances in Clinical Chemistry
日期:2019-01-01
卷期号:: 163-179
被引量:43
标识
DOI:10.1016/bs.acc.2019.03.005
摘要
Pentraxin 3 (PTX3) is involved in vascular inflammation and endothelial dysfunction through various mechanisms. Until now, most studies confirmed an important link between PTX3 and endothelial dysfunction and identified several pathogenetic pathways. PTX3 modulates inflammatory cells, thus stimulating vascular inflammation. Within endothelial cells, it decreases nitric oxide (NO) synthesis, inhibits cell proliferation and alters their functions. PTX3 blocks the effect of fibroblast growth factor 2 (FGF2) by making a molecular complex with these molecules inactivating them. However, there are substances like the tumor necrosis factor-inducible gene 6 protein (TSG-6) that block the PTX3-FGF2 interaction. Interacting with P-selectin, it promotes vascular inflammatory response and endothelial dysfunction. PTX3 also increases the matrix metalloproteinases synthesis directly or by blocking NO synthesis. From a clinical point of view, PTX3 positively correlates with arterial hypertension, flow mediated dilation and, with intima media thickness. Therefore, the involvement of PTX3 in the pathogenesis and evaluation of endothelial dysfunction is clear, and it may become a biomarker in this direction, but further studies are needed to determine its reliability in this direction. Last but not least, PTX3 could become an effective therapeutic target for preventing this dysfunction, but further research needs to be conducted.
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