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首页> 外文期刊>Journal of Reproductive Immunology >FGF-1 and S100A13 possibly contribute to angiogenesis in endometriosis.
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FGF-1 and S100A13 possibly contribute to angiogenesis in endometriosis.

机译：FGF-1和S100A13可能有助于子宫内膜异位症的血管生成。

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Endometriosis is referred often as an angiogenic disease. The pivotal role of angiogenesis in the pathophysiology of this disease has been confirmed by many studies. This process has several steps, and VEGF is probably the most important in its initiation. There are others involved in its continuation and maintenance of the tight balance between a quiescent and activated blood vessel state. In the process of formation of new blood capillaries and arterioles, many different factors are involved in sometimes distinct pathways. Such factors are TGF-beta and endoglin--the latter being one of the main modulators of the TGF-beta signaling pathway. Endoglin is now not only established as a marker of active neo-angiogenesis and activated endothelium, but also turns to be an active player in the very process of endometriotic angiogenesis. Its signaling pathway of hypoxic activation is tightly interconnected with that of VEGF, and also some of the FGFs. FGF-1 and S100A13 are members of two distinct families of proteins -- the FGFs, growth and angiogenic factors, and that of the S100 proteins, -- Ca(2+)-binding proteins involved in cell function regulation, motility and signaling. These two particular members are quite unique in having no signal peptide sequence and being involved in common export pathway. Our hypothesis is that these two factors are involved in vascular remodeling in endometriotic angiogenesis, playing a role in vascular wall formation and migration of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). We believe also that endoglin is tightly involved in the new arteriolar formation in endometriosis, being expressed in VSMCs but not on the ECs of the middle-sized vessels.
机译：子宫内膜异位通常被称为血管生成性疾病。许多研究证实了血管生成在该疾病的病理生理中的关键作用。这个过程有几个步骤，而VEGF可能是其启动过程中最重要的一步。在静态和激活血管状态之间的紧密平衡的持续和维持中，还涉及其他方面。在新的毛细血管和小动脉的形成过程中，许多不同的因素有时参与不同的途径。这些因子是TGF-β和内皮糖蛋白-内皮糖蛋白是TGF-β信号传导途径的主要调节剂之一。现在，内皮糖蛋白不仅被确立为活跃的新血管生成和活化的内皮的标志物，而且在子宫内膜异位血管生成的整个过程中也成为活跃的参与者。其低氧激活的信号传导途径与VEGF以及某些FGF紧密相连。 FGF-1和S100A13是两个不同的蛋白质家族的成员-FGF，生长和血管生成因子，以及S100蛋白质的家族-Ca（2+）结合蛋白参与细胞功能调节，运动和信号传导。这两个特定的成员在没有信号肽序列并且参与共同的输出途径方面非常独特。我们的假设是，这两个因素参与了子宫内膜异位血管生成中的血管重塑，在血管壁的形成以及内皮细胞（ECs）和血管平滑肌细胞（VSMCs）的迁移中起作用。我们还相信内皮糖蛋白与子宫内膜异位症中新的小动脉形成密切相关，在血管平滑肌细胞中表达，但在中型血管的内皮细胞中不表达。

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