How Immune Cells Transform Small Blood Vessels to Larger, More Complex Blood Vessels in Severe Wet Macular Degeneration

Priyatham Mettu, MD
Duke University Eye Center (Durham, NC)

Co-Principal Investigators

Scott W. Cousins, MD
Duke University Medical Center
Year Awarded:
2014
Grant Duration:
July 1, 2014 to June 30, 2016
Disease:
Macular Degeneration
Award Amount:
$120,000
Grant Reference ID:
M2014099
Award Type:
Standard
Award Region:
US Southeastern
Priyatham Mettu, MD

Macrophages Drive Neovascular Remodeling in Neovascular Age-Related Macular Degeneration

Summary

Our research is trying to understand what causes the severe form of wet macular degeneration, a common disease that damages the back of the eye (retina) and is one of the leading causes of blindness in the United States. Macrophages are cells in the body that fight off infection, but in some cases they can cause damage to tissues in the body. We are trying to determine how macrophages make neovascular, or “wet” macular degeneration, worse and harder to treat with available medicines. If we can understand how macrophages make this disease worse, our hope is that we can develop new medicines to treat patients with the disease who otherwise might continue to lose vision.

Details

We are trying to understand what causes the severe form of wet age-related macular degeneration (AMD), one of the leading causes of blindness in the United States. This work is significant because patients with the severe form of the disease do not respond to available medications. Macrophages are cells in the body that fight off infection, but that, in some cases, can cause damage to tissues in the body. We are working to identify the subsets of macrophages in the body that drive the severe form of wet macular degeneration, which is also known as neovascular remodeling. Patients with neovascular remodeling have disease that is characterized by more complex blood vessel structure and scar tissue formation. Using models of new vessel formation, we will identify which subsets drive neovascular remodeling, and what molecule signals they produce to promote disease. We can this use this information to develop new medications that target these macrophage subsets and molecular signals, with the overall goal of improving vision and preventing blindness among patients with severe wet AMD.
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