Why the study?
Do RAS inhibitors targeting cellular Ang II formation prevent retinal damage in patients with diabetic retinopathy?
Do RAS inhibitors targeting cellular Ang II formation prevent retinal damage in patients with diabetic retinopathy?
Understanding the tissue chymase and angiotensin-(1-12) pathways in Ang II formation may provide novel strategies for preventing or treating diabetic retinopathy.
Does not yet support RAS inhibitor use in diabetic retinopathy; leaves open chymase/angiotensin-(1-12) pathways as potential targets.
Diabetic retinopathy (DR) is a major diabetes complication and the leading cause for vision loss and blindness in the adult human population. Diabetes, being an endocrinological disorder dysregulates a number of hormonal systems including the renin angiotensin system (RAS), which thereby may damage both vascular and neuronal cells in the retina. Angiotensin II (Ang II), an active component of the RAS is increased in diabetic retina, and may play a significant role in neurovascular damage leading to the progression of DR. In this review article, we highlight the role of Ang II in the pathogenesis of retinal damage in diabetes and discuss a newly identified mechanism involving tissue chymase and angiotensin-(1-12) [Ang-(1-12)] pathways. We also discuss the therapeutic effects of potential RAS inhibitors targeting blockade of cellular Ang II formation to prevent/ protect the retinal damage. Thus, a better understanding of Ang II formation pathways in the diabetic retina will elucidate early molecular mechanism of vision loss. These concepts may provide a novel strategy for preventing and/or treating diabetic retinopathy, a leading cause of blindness worldwide.
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Ola et al. (2017) studied this question.
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