The aquaporins (AQPs) are integral membrane proteins whose main function is to transport water across cell membranes in response to osmotic gradients. At the ocular surface, AQP1 is expressed in corneal endothelium, AQP3 and AQP5 in corneal epithelium, and AQP3 in conjunctival epithelium. AQPs are also expressed in lens fiber cells (AQP0), lens epithelium (AQP1), ciliary epithelium (AQP1, AQP4) and retinal Müller cells (AQP4). Mutations in AQP0 produce congenital cataracts in humans. Analysis of knockout mice lacking individual AQPs suggests their involvement in maintenance of corneal and lens transparency, corneal epithelial repair, intraocular pressure (IOP) regulation, retinal signal transduction and retinal swelling following injury. The mouse phenotype findings implicate AQPs as potential drug targets for therapy of elevated IOP and ocular disorders involving the cornea, lens and retina. However, much research remains in defining cell-level mechanisms for the ocular AQP functions, in establishing the relevance to human eye disease of conclusions from knockout mice, and in developing AQP-modulating drugs.

中文翻译：

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水通道蛋白在眼睛中的功能。

水通道蛋白 (AQP) 是完整的膜蛋白，其主要功能是响应渗透梯度将水输送到细胞膜上。在眼表，AQP1在角膜内皮中表达，AQP3和AQP5在角膜上皮中表达，AQP3在结膜上皮中表达。AQP 还在晶状体纤维细胞 (AQP0)、晶状体上皮 (AQP1)、睫状上皮 (AQP1、AQP4) 和视网膜穆勒细胞 (AQP4) 中表达。AQP0 的突变会导致人类先天性白内障。对缺乏单个 AQP 的基因敲除小鼠的分析表明，它们参与维持角膜和晶状体透明度、角膜上皮修复、眼内压 (IOP) 调节、视网膜信号转导和损伤后视网膜肿胀。小鼠表型发现表明 AQP 是治疗眼压升高和涉及角膜、晶状体和视网膜的眼部疾病的潜在药物靶点。然而，在确定眼部 AQP 功能的细胞水平机制、确定基因敲除小鼠的结论与人眼疾病的相关性以及开发 AQP 调节药物方面，仍有许多研究。