Summary And Perspective

Multiple AQPs are strongly expressed in ocular tissues, where they appear to serve a variety of functions related to epithelial fluid secretion, regulation of tissue water content, cell migration and proliferation, and neural signal transduction. Small-molecule modulators of AQP function or expression might thus be exploited clinically. At the ocular surface, AQP3 or AQP5 upregulation could accelerate wound healing and reduce corneal edema. Corneal endothelial AQP1-inducers might also reduce corneal edema and associated opacity. Induction of lens AQPs might slow cataract-related opacification. Inhibition of AQP1/AQP4 represents a possible strategy for reducing intraocular pressure associated with glaucoma. In the retina, AQP4 inhibitors might offer neuroprotection following retinal ischemia. These possibilities will require experimental verification in large animal model experiments when nontoxic AQP-selective modulators become available. Aquaporin modulators will also be useful in confirming conclusions from phenotype analysis of knock-out mice.

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