The role of CXC chemokines in the regulation of angiogenesis.
The role of CXC chemokines in the regulation of angiogenesis.
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DOI：
10.1159/000058728
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发表时间：
1999-07
影响因子：
--
通讯作者：
M. Keane;R. Strieter
中科院分区：
文献类型：
--
作者：
M. Keane;R. Strieter
血管新生是指从原有血管中生长出新的血管系统。这是一个重要的生物过程的中心，各种生理和病理过程。血管生成的调节依赖于促进（血管生成因子）或抑制（血管抑制因子）新生血管的局部因子的双重，但相反的平衡。例如，成人正常毛细血管内皮细胞的周转率通常以月或年为单位测量，这表明在稳态条件下，血管生成因子和血管抑制因子存在等效平衡的潜力。相比之下，在伤口修复和肉芽组织的发育过程中，这种平衡倾向于血管生成因子的优势，导致在几天内建立新的功能毛细血管。伤口相关的血管生成是局部控制和短暂的。随着伤口新生血管的迅速形成，这些新生血管实际上消失了，使组织血管系统恢复到体内平衡的环境。在伤口修复解决的背景下，血管生成的突然终止支持了以下观点，即在局部环境中发生：血管生成因子的显著减少和/或抑制新生血管形成的因子水平同时增加。与伤口修复过程中血管生成的精确调控相反，血管生成的失调会导致血管生成和血管抑制因子之间的关系失衡，从而促进持续的净血管生成，从而导致慢性炎症和实体瘤的生长。血管生成和血管抑制因子的补体在不同的生理和病理环境中可能有所不同。然而，认识到这一点
Angiogenesis is defined as the growth of neovasculature from preexisting vessels. This is an important biological process central to a variety of physiologic and pathologic processes. The regulation of angiogenesis depends upon a dual, yet opposing balance of local factors which promote (angiogenic factors) or inhibit (angiostatic factors) neovascularization. For example, the rate of normal capillary endothelial cell turnover in adults is typically measured in months or years, suggesting the potential of an equivalent balance in the presence of both angiogenic and angiostatic factors under homeostatic conditions. By contrast, during wound repair and development of granulation tissue, this balance shifts in favor of a predominance of angiogenic factors leading to establishment of new functioning capillaries within a matter of days. Woundassociated angiogenesis is locally controlled and transient. As rapidly as neovascularization occurs in the wound, these neovessels virtually disappear, returning the tissue vasculature to a homeostatic environment. This abrupt termination of angiogenesis in the context of the resolution of wound repair supports the notion that the following occurs in the local environment: a marked reduction in the elaboration of angiogenic factors and/or a simultaneous increase in the levels of factors that inhibit neovascularization. In contrast to the precise regulation of angiogenesis of wound repair, dysregulation of angiogenesis can lead to an imbalance in the relationship of angiogenic and angiostatic factors that favors persistent net angiogenesis that contributes to the pathogenesis of chronic inflammation and solid tumor growth. The complement of angiogenic and angiostatic factors may vary among different physiologic and pathologic settings. However, the recognition of this