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未来抗青光眼治疗的靶标分子:TGF-β可能发挥作用。

Future target molecules in antiglaucoma therapy: tgf-Beta may have a role to play.

机构信息

Department of Pharmacology, Faculty of Medicine, Universiti Teknologi MARA, Shah Alam, Malaysia.

出版信息

Ophthalmic Res. 2010;43(1):1-10. doi: 10.1159/000246571. Epub 2009 Oct 14.

Abstract

Glaucoma, a leading cause of irreversible blindness, is often associated with increased resistance to aqueous outflow in trabecular tissue. Increased outflow resistance has been attributed to increased extracellular matrix (ECM) deposition in trabecular tissue. A critical balance between the synthesis and breakdown of the components of extracellular tissue is important in keeping the intraocular pressure within the normal range. Multiple mechanisms have been shown to affect ECM turnover in trabecular tissue. In this review, we examine the related literature to understand the role of TGF-beta in ECM turnover, in the development and progression of glaucoma, and in possible therapeutic strategies that can be devised by targeting the TGF-beta signaling pathways.

摘要

青光眼是导致不可逆性失明的主要原因之一,通常与小梁组织中房水流出阻力增加有关。房水流出阻力的增加归因于小梁组织中细胞外基质(ECM)的沉积增加。细胞外组织成分的合成和分解之间的关键平衡对于将眼内压维持在正常范围内非常重要。已经有多种机制表明可以影响小梁组织中的 ECM 周转。在这篇综述中,我们研究了相关文献,以了解 TGF-β在 ECM 周转、青光眼的发展和进展中的作用,以及通过靶向 TGF-β信号通路设计可能的治疗策略。

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