摘要
血小板反应蛋白(TSP)1/2是血管化有效的内源性抑制因子,通过拮抗血管内皮生长因子抑制内皮细胞的迁移、增殖,并促其凋亡,其作用靶点为CD36、CD47和整合素。而CD36和β整合素是信号转导的起始环节,CD36和CD47的血管化抑制作用与一氧化氮通路相关。研究TSP1/2及其类似物的作用机制有助于研究抗癌新疗法以及治疗其他与血管化相关的疾病。该文重点阐释TSP1/2与血管内皮细胞相互作用调节血管化的分子作用机制以及TSP1/2及其类似物在抗肿瘤、组织损伤修复等领域的临床应用进展。
Thrombospondin (TSP) -1 and TSP-2 are potent endogenous inhibitors of angiogenesis. They inhibit angiogenesis through direct effects on endothelial cell migration, proliferation, survival, and apoptosis by antagonizing the activity of vascular endothelial growth factor. TSP-1 and TSP-2 exert their direct effects through CD36, CD47 and integrins. CD36 and 13 integrin are the starting point of the signal transduction ,while the anti-angiogensis role of CD36 and CD47 are associated with nitric oxide pathway. Advances in understand- ing of the molecular regulation of angiogenesis by TSP1/2 have paved the way for innovations in experimental treatment of cancers and will likely continue to offer vast avenues for discovery in other angiogenesis related disease processes as well. Here is to make a review of the progress of the molecular mechanisms of TSP1/2 and vascular endothelial cell interactions regulating angiogenesis and the clinical application of TSP1/2 and its analogues in anti-tumar and tissue damage repair.
出处
《医学综述》
2016年第9期1669-1673,共5页
Medical Recapitulate
基金
上海市科学技术委员会科研计划项目(14ZR1433100)