Regenfuss Birgit, Bock Felix, Parthasarathy Anand, Cursiefen Claus
Department of Ophthalmology and Interdisciplinary Center for Clinical Research (IZKF), Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany.
Lymphat Res Biol. 2008;6(3-4):191-201. doi: 10.1089/lrb.2008.6348.
The normal cornea, the transparent "windscreen" of the eye, is devoid of both blood and lymphatic vessels. Nevertheless, both hem- and lymphangiogenesis can occur in response to severe corneal inflammation and can lead to blindness. Judah Folkman and co-workers exceedingly used the normally avascular cornea as the in vivo model system to study the mechanisms of angiogenesis and to test activators and inhibitors of angiogenesis in the last 3 decades. Recently, the cornea also became a successful model to study especially inflammatory lymphangiogenesis. As the last step in the circle from bedside to bench and back, we now are seeing the first (usually off-label) use of specific novel angiogenesis inhibitors in the diseased and pathologically vascularized human cornea to treat sight-threatening corneal angiogenesis and to promote graft survival after corneal transplantation by inhibiting lymphangiogenesis.
正常角膜，即眼睛的透明“挡风玻璃”，既没有血管也没有淋巴管。然而，在严重的角膜炎症反应中，血管生成和淋巴管生成均可能发生，并可能导致失明。在过去三十年里，朱达·福克曼及其同事极大地利用了正常无血管的角膜作为体内模型系统来研究血管生成机制，并测试血管生成的激活剂和抑制剂。最近，角膜也成为了一个成功的模型，尤其用于研究炎症性淋巴管生成。作为从床边到实验室再回到床边这一循环的最后一步，我们现在看到了特定新型血管生成抑制剂首次（通常为超说明书用药）用于患病且病理性血管化的人类角膜，以治疗威胁视力的角膜血管生成，并通过抑制淋巴管生成来促进角膜移植后的移植物存活。
