口腔扁平苔藓血管生成:与不同侵袭程度病变的比较研究

K. Cherubini, V. D. Silva, T. G. Lopes, M. A. Figueiredo, F. Salum, M. Payeras
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引用次数: 2

摘要

血管生成是指由原有血管结构形成新血管的过程,它受多种生长因子和促血管生成细胞因子以及各种内源性血管生成抑制剂的控制。在生理情况下,这些激活剂和抑制剂处于平衡状态,但在病理情况下,促血管生成剂[1]可能持续或过度激活。血管内皮生长因子(Vascular endothelial growth factor, VEGF)是已知的最有效的血管生成刺激因子之一,除了内皮细胞的增殖和迁移外,还具有诱导血管通透性[2]的能力,这是新血管[3]形成的重要步骤。其他对血管形成至关重要的生长因子是血管生成素(angiopoietin, ANG),其中ang1和ang2是最知名和最具特征的。与VEGF相反,血管生成素是血管生成介质,其作用不会诱导内皮细胞有丝分裂活性。尽管它们的生物学活性尚未完全阐明,但已知ANG-1在血管静止的情况下以及血管成熟的过程中不断分泌,血管成熟是血管生成的后期步骤[5,6]。此外,ANG-1作为抗炎细胞因子[4]。另一方面,尽管ANG-2与ANG-1具有相同的Tie-2受体亲和性,但不会使其磷酸化,从而对ANG-1[4]产生拮抗作用,破坏血管内皮的稳定,导致新生血管的退化和内皮细胞的凋亡
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Angiogenesis in Oral Lichen Planus: A Comparative Study with Lesions of Different Degrees of Aggressiveness
Angiogenesis, the process by which new vessels are formed from pre-existing vascular structures, is controlled by numerous growth factors and pro-angiogenic cytokines, as well as by various endogenous inhibitors of neovascularization. under physiological situations, these activators and inhibitors are in balance, but in pathological situations there can be persistent or excessive activation of pro-angiogenic agents [1]. Vascular endothelial growth factor (VEGF) is one of the most potent and known stimulators of angiogenesis, showing the ability to induce vascular permeability [2], besides the proliferation and migration of endothelial cells, essential steps for the development of new blood vessels [3]. Other growth factors essential for vascular formation are the angiopoietins (ANG), among which ANG-1 and ANG-2 are the most known and best characterized [4]. In contrast to VEGF, angiopoietins are angiogenic mediators whose action does not induce mitotic activity in endothelial cells [5]. Despite their biological activities not being completely elucidated, it is known that ANG-1 is constantly secreted in situations of vascular quiescence, as well as during the process of vascular maturation, a later step in angiogenesis [5,6]. Besides, ANG-1 acts as an anti-inflammatory cytokine [4]. On the other hand, ANG-2, despite showing affinity for the same Tie-2 receptor of ANG-1, does not phosphorylate it, thus exerting an antagonistic effect of ANG-1 [4], destabilizing the vascular endothelium, which causes the regression of neoformed vessels and apoptosis in endothelial Crimson Publishers Wings to the Research Research Article
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