Activating the Eye’s Own Nitric Oxide to Fight Glaucoma

The goal of this project is to develop safer, longer-lasting glaucoma treatments by restoring the eye’s own nitric oxide (NO) production. By targeting tiny sensory organelles called primary cilia with a selective enzyme inhibitor, we seek to enhance fluid drainage and lower eye pressure naturally.

We aim to develop safer, longer-lasting glaucoma treatments by restoring the eye’s own nitric oxide (NO) production. By targeting tiny sensory organelles called primary cilia with a selective enzyme inhibitor, we seek to enhance fluid drainage and lower eye pressure naturally.

This project establishes primary cilia as an upstream, therapeutically targetable regulator of nitric oxide production in the eye’s fluid drainage pathway. It introduces a strategy to restore cilia function and enhance the eye’s own nitric oxide signaling for intraocular pressure control. By combining real-time imaging with functional approaches, this work enables direct visualization of dynamic nitric oxide regulation and provides a new framework for developing therapies that harness endogenous signaling mechanisms.

This study aims to develop a new way to lower eye pressure by boosting the eye’s own natural nitric oxide production rather than relying on externally supplied drugs. By targeting primary cilia, this approach could lead to safer, longer-lasting treatments that better preserve vision in patients with glaucoma. In addition, it will advance our understanding of how the eye senses and regulates pressure, opening new directions for research on pressure control and disease prevention.