Vascular injury and modulation of MAPKs: a targeted approach to therapy of restenosis.
Vascular injury and modulation of MAPKs: a targeted approach to therapy of restenosis.
复制标题
血管损伤和 MAPK 调节：再狭窄治疗的靶向方法。
DOI：
10.1016/j.cellsig.2007.03.002
复制
发表时间：
2007
影响因子：
4.8
通讯作者：
Pintucci,Giuseppe
中科院分区：
文献类型：
--
作者：
Yu,Pey-Jen;Ferrari,Giovanni;Pirelli,Luigi;Gulkarov,Iosif;Galloway,AubreyC;Mignatti,Paolo;Pintucci,Giuseppe
恢复缺血区域血液循环的心血管介入治疗伴随着显著的组织损伤，这会引发可能导致血管再狭窄的血管重塑反应。早期内皮功能障碍和/或损伤是级联反应的早期事件，其通过炎症反应和具有大量细胞外基质沉积的中膜平滑肌细胞的去分化导致内膜增生。在这里，我们提出了继发于血管损伤的内膜增生的分子和细胞机制，并讨论了细胞内信号通路的治疗调制的潜在作用，差异影响血管内皮细胞和平滑肌细胞。丝裂原活化蛋白激酶（MAPKs）的作用及其在这些过程中的调制结果在这里强调，因为它们提供了一个有前途的治疗靶点，用于预防再狭窄。
Cardiovascular interventions that restore blood circulation to ischemic areas are accompanied by significant tissue damage, which triggers a vascular remodeling response that may result in restenosis of blood conduits. Early endothelial dysfunction and/or impairment is the early event of a cascade that leads, through an inflammatory response and dedifferentiation of medial smooth muscle cells with abundant deposition of extracellular matrix, to intimal hyperplasia. Here we present the molecular and cellular mechanisms of intimal hyperplasia secondary to vascular injury and discuss the potential role of therapeutic modulation of the intracellular signaling pathways that differentially effect vascular endothelial and smooth muscle cells. The role of mitogen-activated protein kinases (MAPKs) and the outcome of their modulation in these processes are highlighted here as they provide a promising therapeutic target for prevention of restenosis.