Diabetic retinopathy (DR) is a microvascular complication of diabetes. The retinal pigment epithelium (RPE) forms the outer layer of the blood‑retinal barrier and serves a role in maintaining retinal function. RPE cell injury has been revealed in diabetic animal models, and high glucose (HG) levels may cause damage to RPE cells by increasing the levels of oxidative stress, promoting pro‑inflammatory gene expression, disrupting cell proliferation, inducing the endothelial‑mesenchymal transition, weakening tight conjunctions and elevating cell death mechanisms, such as apoptosis, ferroptosis and pyroptosis. Non‑coding RNAs including microRNAs, long non‑coding RNAs and circular RNAs participate in RPE cell damage caused by HG levels, which may provide targeted therapeutic strategies for the treatment of DR. Plant extracts such as citrusin and hesperidin, and a number of hypoglycemic drugs, such as sodium‑glucose co‑transporter 2 inhibitors, metformin and glucagon‑like peptide‑1 receptor agonists, exhibit potential RPE protective effects; however, the detailed mechanisms behind these effects remain to be fully elucidated. An in‑depth understanding of the contribution of the RPE to DR may provide novel perspectives and therapeutic targets for DR.
Keywords: cell injury; diabetic retinopathy; drugs; non‑coding RNAs; retinal pigment epithelium cell.