Taubman M B
Department of Medicine, Mt. Sinai School of Medicine, New York, New York 10029.
Am J Cardiol. 1993 Sep 9;72(8):55C-60C. doi: 10.1016/0002-9149(93)90256-c.
In response to vascular injury, such as occurs in acute or chronic atherosclerosis, vascular smooth muscle cells (VSMCs) proliferate and migrate, ultimately contributing to vessel narrowing. Several growth agonists, including platelet-derived growth factor and fibroblast growth factor, are known to cause VSMCs to proliferate and are believed to be present at sites of vessel injury. Targets for inhibiting VSMC growth or migration in the presence of multiple growth agonists include genes that are induced in common by VSMC growth factors. This article summarizes the in vivo and in vitro findings of experiments designed to investigate the regulation of tissue factor in VSMCs in 2 animal models. The findings demonstrate that tissue factor is rapidly induced by growth factors in VSMC culture and by balloon injury in aortic media, and they suggest that VSMCs may play a major role in mediating the early thrombotic response. Strategies designed to inhibit the response of VSMCs to growth agonists may therefore have important implications for the treatment of intravascular thrombosis.
针对血管损伤，如急性或慢性动脉粥样硬化中发生的损伤，血管平滑肌细胞（VSMC）会增殖并迁移，最终导致血管狭窄。已知几种生长激动剂，包括血小板衍生生长因子和成纤维细胞生长因子，可导致VSMC增殖，并被认为存在于血管损伤部位。在多种生长激动剂存在的情况下，抑制VSMC生长或迁移的靶点包括VSMC生长因子共同诱导的基因。本文总结了旨在研究两种动物模型中VSMC组织因子调节的体内和体外实验结果。研究结果表明，生长因子在VSMC培养中以及主动脉中膜的球囊损伤可迅速诱导组织因子，并且提示VSMC可能在介导早期血栓形成反应中起主要作用。因此，旨在抑制VSMC对生长激动剂反应的策略可能对血管内血栓形成的治疗具有重要意义。
