Ischemic retinopathies (IR) were vision-threatening disorders that afflicted many people globally. Photocoagulation and anti-VEGF therapy were 2 current treatment methods with negative effects and were often ineffective in preventing disease development. As a result, additional molecular targets should be considered to develop novel therapy techniques that were both safer and more effective. During the onset of IR, the retina, which was generally immune-privileged, was exposed to increased cellular stress and inflammation levels, which attracted and activated resident mononuclear phagocytes (MPs) from the bloodstream (microglia). Activated MPs had a wide range of functions in the retinal tissue, with the ability to both oppose and worsen the detrimental tissue microenvironment. The current study examined what was known about the function of inflammation and activated retinal MPs in the 2 most common IRs, retinopathy of prematurity and diabetic retinopathy. MPs and their secreted factors and cell-cell interactions between MPs and endothelial cells were of particular interest. Researchers concluded that activated MPs played a key role in the onset and progression of IRs, and hence could be a promising new target for novel pharmaceutical interventions in these diseases.
