Vascular wall growth control: the role of the endothelium.
Vascular wall growth control: the role of the endothelium.
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DOI：
10.1161/01.atv.1.2.107
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发表时间：
1981-03
期刊：
影响因子：
--
通讯作者：
S. Schwartz;C. Gajdusek;S. Selden
中科院分区：
文献类型：
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作者：
S. Schwartz;C. Gajdusek;S. Selden
目前我们对内皮细胞生长的调控以及内皮细胞损伤在动脉粥样硬化发病机制中的作用的认识可以概括如下：1。内皮细胞可以在不存在外源性生长因子的情况下在血浆来源的血清中生长。这与大多数其他非转化细胞的生长要求完全不同。然而，这些因素可能会延长复制寿命，并增加内皮细胞在稀疏密度下生长的能力。这些现象与体内内皮生长控制的相关性尚不清楚。没有证据表明伤口边缘再生需要外源性生长因子。鉴于相对缺乏生长因子的要求，这是有趣的考虑内皮细胞生长的关键控制因素是细胞接触的可能性。2.内皮细胞再生可能依赖于内皮细胞运动。这种关系的性质可能是重要的，在控制内皮细胞再生的能力，在不同的流动条件下，病变周围或在血管树的不同部分，并在确定内皮细胞的能力，以响应结缔组织覆盖病变的变化。3.体内的内皮细胞能够非常迅速地再生小面积的剥脱。这一过程可能足够快，以允许内皮细胞取代死亡细胞，因为他们正在失去，导致脱落而不剥脱。4.我们几乎没有证据表明内皮剥脱是自发的，或者是在动脉粥样硬化危险因素的作用下，直到病变形成开始。这并不排除发生小的、重复的、短暂的剥脱事件并在动脉粥样硬化病变的起始中起作用的可能性。然而，重要的是开始考虑非剥脱性损伤在动脉粥样硬化中的作用。5.动脉粥样硬化中血栓形成的事实意味着内皮完整性的最终破坏。这种崩溃的机制仍然未知。6.最后，平滑肌细胞和内皮细胞在生长控制水平上的相互作用是一个问题。这包括有证据表明，有一个临界量的内皮细胞，必须失去损伤形成之前，刺激和最近的证据表明，内皮细胞产生的物质能够调节平滑肌细胞的生长。
The current state of our knowledge of the control of endothelial growth and the role of endothelial injury in the pathogenesis of atherosclerosis can be summarized as follows: 1. Endothelial cells can be grown in plasma-derived serum in the absence of exogenous growth factors. This is quite different from the growth requirements of most other nontransformed cells. These factors may, however, prolong replicative life span and increase the ability of endothelium to grow at sparse density. The relevance of these phenomena to the control of endothelial growth in vivo is unclear. There is no evidence that exogenous growth factors are required for wound edge regeneration. In view of the relative lack of growth factor requirements, it is intriguing to consider the possibility that the critical control factor for endothelial cell growth is cell contact. 2. Endothelial cell regeneration may be dependent on endothelial cell motility. The nature of this relationship may be important in controlling the ability of the endothelium to regenerate itself under different flow conditions around lesions or in different parts of the vessel tree and in determining the ability of the endothelium to respond to changes in the connective tissue overlying lesions. 3. Endothelial cells in vivo are able to regenerate small areas of denudation extremely rapidly. This process may be sufficiently rapid to permit the endothelium to replace dying cells as they are being lost, resulting in desquamation without denudation. 4. We have little evidence for endothelial denudation either spontaneously or in response to atherosclerosis risk factors until after lesion formation has begun. This does not rule out the possibility that small, repeated, transient episodes of denudation occur and play a role in the initiation of atherosclerotic lesions. It is important, however, to begin considering the role of nondenuding injuries in atherosclerosis. 5. The fact that thrombosis occurs in atherosclerosis implies an eventual breakdown of endothelial integrity. The mechanism of that breakdown remains unknown. 6. Finally, there is the question of interactions between smooth muscle cells and endothelial cells at the level of growth control. This includes the evidence that there is a critical amount of endothelium that must be lost before lesion formation is stimulated and the recent evidence that endothelial cells produce substances able to regulate growth of smooth muscle cells.