Schwartz S M, Liaw L
Department of Pathology, University of Washington, School of Medicine, Seattle.
J Cardiovasc Pharmacol. 1993;21 Suppl 1:S31-49. doi: 10.1097/00005344-199321001-00007.
We briefly review and compare the current knowledge of growth mechanisms for the mitogenic response of endothelial cells and smooth-muscle cells to injury. For the endothelium, this focuses on the evidence that growth control involves two components: an endogenous inhibition mechanism, which can be overcome either by fibroblast growth factor (FGF) or by other agents that disrupt cell-cell junctions, and a separate mechanism, which requires FGF to allow cells to respond to a mitogenic effect. The smooth-muscle cell story is more complex; however, there is evidence here as well of an endogenous inhibitory mechanism, which may be overcome by a wide variety of agents. Platelet-derived growth factor, long seen as a major mitogen, does not itself now appear to be a major mitogen in vivo. In contrast, FGF also seems to play a major role in initiating smooth-muscle replication. Other molecules, including angiotensin II, bradykinin, thrombin, and catecholamines, are beginning to appear to play major roles in control of smooth-muscle replication in vivo as well.
我们简要回顾并比较了目前关于内皮细胞和平滑肌细胞对损伤产生有丝分裂反应的生长机制的知识。对于内皮细胞，这集中在以下证据上：生长控制涉及两个成分，一种内源性抑制机制，它可以被成纤维细胞生长因子（FGF）或其他破坏细胞间连接的因子所克服；以及一种独立的机制，它需要FGF使细胞对有丝分裂效应作出反应。平滑肌细胞的情况更为复杂；然而，这里也有内源性抑制机制的证据，它可能被多种因子所克服。长期以来被视为主要促有丝分裂原的血小板衍生生长因子，现在看来在体内本身并不是主要的促有丝分裂原。相比之下，FGF似乎在启动平滑肌复制中也起主要作用。其他分子，包括血管紧张素II、缓激肽、凝血酶和儿茶酚胺，在体内控制平滑肌复制方面似乎也开始发挥主要作用。
