New research has revealed a specific pathway responsible for the formation of abnormal blood vessels that can cause blindness in age-related macular degeneration, according to a study published in the journal Nature Communications.

In previous studies, interleukin-10 (IL10) has been shown to contribute to the formation of blood vessels in wet macular degeneration; the “wet” form is more often associated with blindness than the “dry” form. Increased levels of IL10 promote the proliferation of specific immune cells, called M2 macrophages, which in turn create damaging blood vessel growth under the retina.

Principal investigator and retina specialist Rajendra S. Apte, MD, PhD, and colleagues from the Washington University School of Medicine in St. Louis, engineered mice with various disabled cell-signaling pathways. A series of experiments led to the discovery of STAT3, a protein abundant in M2 macrophages that activates and alters immune cells in the eye, promoting the formation of abnormal blood vessels. Further examination of eye tissue from patients who underwent surgery for wet macular degeneration in the 1980s and 1990s also showed presence of the STAT3 protein.

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Study findings suggest M2 macrophages with active STAT3 are responsible for damaging blood vessel growth in both mice and humans. With a better understanding of macular degeneration at a molecular level, compounds used to disrupt the actions of STAT3 in mice may be viable to halt or reverse vision loss in humans, researchers concluded.

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