Diabetic macular edema is the major cause of vision impairment in patients with non-proliferative diabetic retinopathy. Thickness and pathological alterations in each retina layer of diabetic macular edema (DME) patients can be performed by optical coherence tomography (OCT) device. And retinal light sensitivity at specific retinal point and fixation state can be detected by microperimetry qualitatively and quantitatively. Moreover, OCT can discover pathological anatomical changes in the retina of DME patients, thus facilitating the interpretation of the structure-function relationship in DME with combination of microperimetry results. At present, there are various therapies for DME patients, and the primary method in evaluating therapeutic efficacy is to compare the pathological changes in the retina before and after treatment by OCT. Besides, microperimetry can provide information in visual function restoration. The combined application of OCT and microperimetry has broad prospects in the diagnosis and treatment of DME patients.
Integrins is a family of multi-functional cell-adhesion molecules, heterodimeric receptors that connect extracellular matrix to actin cytoskeleton in the cell cortex, thus regulating various physiological and pathological processes. Risuteganib (Luminate®) is a novel broad-spectrum integrin inhibitor. Based on multiple biological functions of anti-angiogenesis, vitreolysis, and neuroprotection, risuteganib is hopeful in treating several fundus diseases such as diabetic macular edema, vitreomacular traction, and non-exudative age-related macular degeneration. By far, risuteganib has successfully met the endpoints for three phase 2 studies and is preparing to enter the phase 3 of diabetic macular edema clinical trials. Overall the risuteganib is safe with no serious ocular or systemic adverse events. Given the unique mechanism of action and longer duration of efficacy, intravitreal injection of risuteganib has the potential to serve as a primary therapy, or adjunctive therapy to anti-VEGF agents.
Uric acid (UA) is the final product of human purine metabolism. As one of the main antioxidants in the body, it can scavenge oxidative radicals. Under the action of oxidative-antioxidant shuttle mechanism, the antioxidant activity of UA can be reversed, causing inflammation and oxidative stress of vascular endothelial cells. Hyperuricemia (HUA) is considered to be one of the major risk factors for diabetes and diabetic nephropathy. The study of HUA in diabetic retinopathy (DR) is also a hot topic. UA can cause retinal vascular sclerosis, and affect the occurrence and development of DR by promoting oxidative stress and inducing neovascularization.