BCL6B作为绒毛膜视网膜血管病变治疗靶点的潜力。

Shinsuke Nakamura, Hideaki Hara
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引用次数: 0

摘要

眼部组织是人体血管密度最大的组织之一,血管病变是许多眼部疾病中视力下降和视野缺损的一个因素。目前,以血管内皮生长因子(VEGF)为靶点的药物是治疗眼内血管病变的首选药物,然而,在某些情况下,它们并不是完全有效的。因此,我们探索除VEGF以外的致病分子,旨在开发新的分子靶向治疗。通过模拟眼内血管病变的实验病理模型,我们发现B细胞CLL/淋巴瘤6成员B蛋白(BCL6B)可能在眼内血管生成和血管高通透性中发挥重要作用,该蛋白已被确定为brick -a-brac、Tramtrack和Broad复合物蛋白。在本文中,我们介绍了抑制BCL6B表达的有效性,并讨论了通过靶向Notch信号在绒毛膜视网膜血管病变中发现药物的可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[The potential of BCL6B as a therapeutic target for chorioretinal vascular lesions].

The ocular tissue is one of the most densely populated tissues in the body with extremely small blood vessels, and vascular lesions have been reported to be a factor in vision loss and visual field defects in many ocular diseases. Currently, vascular endothelial growth factor (VEGF)-targeted agents are the first line of treatment for intraocular vascular lesions, however, there are some cases in which they are not fully effective. Therefore, we explored pathogenic molecules other than VEGF, aiming to develop new molecular-targeted therapy. Using an experimental pathological model mimicking intraocular vascular lesions, we found that B-cell CLL/lymphoma 6 member B protein (BCL6B), which has been identified as a Bric-a-brac, Tramtrack, and Broad Complex protein, may play an important role in intraocular angiogenesis and vascular hyperpermeability. In this article, we introduce the usefulness of suppressing BCL6B expression and discuss the possibility of drug discovery by targeting Notch signaling in chorioretinal vascular lesions.

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来源期刊
Folia Pharmacologica Japonica
Folia Pharmacologica Japonica Pharmacology, Toxicology and Pharmaceutics-Pharmacology
CiteScore
0.40
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0.00%
发文量
132
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