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Key mechanism of intraocular pressure regulation suggests novel treatment approaches for glaucoma

Key Takeaways

  • Researchers have discovered a new mechanism of intraocular pressure regulation. 
  • The findings may pave the way for novel treatment approaches for glaucoma, with the aspiration of preventing vision loss from this disease

In many glaucoma patients, the fluid within the eye (known as “aqueous humor”) builds up, resulting in higher intraocular pressure (IOP, the amount of pressure or force inside of your eyes). Long-term medication is required to control high IOP. However, current drugs have limitations in that they can only slow glaucoma progression rather than halt it completely. Drugs may also have suboptimal tolerability and their efficacy diminishes over time.

According to a press release from The Hong Kong Polytechnic University (PolyU), Dr. Samantha Shan, Research Assistant Professor of the School of Optometry at PolyU and her team have discovered a key mechanism of IOP regulation. The findings may pave the way for novel treatment approaches for glaucoma, with the aspiration of preventing vision loss from this disease. 

Specifically, the team has identified thrombospondin-1 (TSP-1) as a protein that reduces the outflow of aqueous humor and increases IOP. They further found that by mimicking certain microRNAs, the name of a family of molecules that helps cells control the kinds and amounts of proteins they make, in human trabecular meshwork (hTM) cells, which are responsible for draining aqueous humor within the eye, they could reduce the levels of TSP-1.

Looking forward, the team will investigate the direct interaction between specific microRNAs and TSP-1. They will also examine the functional consequences of modulating this pathway on aqueous humor outflow and IOP regulation in animals. This would be achieved by utilizing eye injections of a TSP-1 target-specific blocker or microRNA mimics in mouse eyes.

Edited by Miriam Kaplan, PhD

Source: Hong Kong Polytechnic University, Medical Xpress, July 25, 2024; see source article