Abstract
Diabetic retinopathy (DR) is a frequent microvascular complication of advanced-stage diabetes. Endothelial cell dysfunction (ED) induced by diabetes plays an important role in the development of DR. It is considered that inflammation and mitochondrial homeostasis are associated with the progression of ED. Takeda G protein-coupled receptor 5 (TGR5) is a membrane receptor for bile acids (BAs) that plays an important role in regulating BA metabolism. Recent studies have shown that TGR5 is involved in regulating various mediators of ED and improving the dysfunction of vascular endothelial cells in DR; however, the exploration of specific related mechanisms remains an active research area in this field, which suggests that TGR5 may be one of the potential targets for the treatment of associated ED in DR. In the present review, the association between TGR5 and mitochondrial homeostasis was investigated. The extent of inflammation in DR-induced ED was assessed to provide possible evidence for the development of targeted therapies against DR.
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