再狭窄
血管成形术
医学
支架
内皮祖细胞
祖细胞
冠状动脉疾病
心脏病学
内皮
血栓形成
内皮功能障碍
冠状动脉
内皮干细胞
动脉
干细胞
外科
内科学
细胞生物学
生物
体外
生物化学
作者
Kim Van der Heiden,Frank Gijsen,Andrew Narracott,Sarah Hsiao,Ian Halliday,Julian Gunn,Jolanda J. Wentzel,Paul C. Evans
摘要
Stent deployment following balloon angioplasty is used routinely to treat coronary artery disease. These interventions cause damage and loss of endothelial cells (EC), and thus promote in-stent thrombosis and restenosis. Injured arteries are repaired (intrinsically) by locally derived EC and by circulating endothelial progenitor cells which migrate and proliferate to re-populate denuded regions. However, re-endothelialization is not always complete and often dysfunctional. Moreover, the molecular and biomechanical mechanisms that control EC repair and function in stented segments are poorly understood. Here, we propose that stents modify endothelial repair processes, in part, by altering fluid shear stress, a mechanical force that influences EC migration and proliferation. A more detailed understanding of the biomechanical processes that control endothelial healing would provide a platform for the development of novel therapeutic approaches to minimize damage and promote vascular repair in stented arteries.
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