Taubman M B
Department of Medicine, Mount Sinai School of Medicine, New York, NY.
Thromb Haemost. 1993 Jul 1;70(1):180-3.
VSMC have been long thought to play a critical role in restenosis by proliferating and migrating from the vessel media to the intima, resulting in intimal hyperplasia. Recently, it has been suggested that the VSMC may play an earlier role in the events leading to restenosis, for example through the production of PDGF. The work described above suggests that the VSMC may mediate both the early inflammatory and thrombotic responses associated with vessel injury. Thus the VSMC may be involved in all phases of vascular injury, including thrombosis, inflammation, and intimal hyperplasia. Additional work will be necessary to fully elucidate the programs activated in VSMC in response to growth and migratory factors. The recent advances in recombinant DNA technology provide the hope that this will lead to novel approaches to attenuate the response of the VSMC to injury.
长期以来，人们一直认为血管平滑肌细胞（VSMC）通过从血管中膜增殖并迁移至内膜，导致内膜增生，在再狭窄中起关键作用。最近，有人提出VSMC可能在导致再狭窄的事件中发挥更早的作用，例如通过产生血小板衍生生长因子（PDGF）。上述研究表明，VSMC可能介导与血管损伤相关的早期炎症和血栓形成反应。因此，VSMC可能参与血管损伤的所有阶段，包括血栓形成、炎症和内膜增生。需要开展更多工作来全面阐明VSMC在对生长和迁移因子作出反应时所激活的程序。重组DNA技术的最新进展带来了希望，即这将导致采用新方法来减弱VSMC对损伤的反应。
