Abstract
Diabetes mellitus (DM) has become a vital societal problem as epidemiological studies demonstrate the increasing incidence of type 1 and type 2 diabetes. Lesions observed in the retina in the course of diabetes, referred to as diabetic retinopathy (DR), are caused by vascular abnormalities and are ischemic in nature. Vascular lesions in diabetes pertain to small vessels (microangiopathy) and involve precapillary arterioles, capillaries and small veins. Pericyte loss, thickening of the basement membrane, and damage and proliferation of endothelial cells are observed. Endothelial cells (monolayer squamous epithelium) form the smooth internal vascular lining indispensable for normal blood flow. Breaking its continuity initiates blood coagulation at that site. The endothelium controls the process of exchange of chemical substances (nutritional, regulatory, waste products) between blood and the retina, and blood cell passing through the vascular wall. Endothelial cells produce biologically active substances involved in blood coagulation, regulating vascular wall tension and stimulating neoangiogenesis. On the other hand, recent studies have demonstrated that diabetic retinopathy may be not only a microvascular disease, but is a result of neuroretinal degeneration. Neuroretinal degeneration appears structurally, as neural apoptosis of amacrine and Muller cells, reactive gliosis, ganglion cell layer/inner plexiform (GCL) thickness, retinal thickness, and retinal nerve fiber layer thickness, and a reduction of the neuroretinal rim in minimum rim width (MRW) and functionally as an abnormal electroretinogram (ERG), dark adaptation, contrast sensitivity, color vision, and microperimetric test. The findings in early stages of diabetic retinopathy may precede microvascular changes of this disease. Furthermore, the article’s objective is to characterize the factors and mechanisms conducive to microvascular changes and neuroretinal apoptosis in diabetic retinopathy. Only when all the measures preventing vascular dysfunction are determined will the risk of complications in the course of diabetes be minimized.
Highlights
Diabetes mellitus (DM) has become a major societal problem
No statistically significant differences were demonstrated in the level of vascular endothelial growth factor (VEGF) between the group of patients with T1DM, retinopathy and nephropathy but without hypertension compared to a healthy control [53]
advanced glycation end products (AGEs)-receptor for AGEs (RAGE) axis plays a crucial role in the sustained inflammation, neurodegeneration, and retinal microvascular dysfunction occurring during diabetic retinopathy [58,59]
Summary
Diabetes mellitus (DM) has become a major societal problem. Epidemiological studies demonstrate the increasing incidence of type 1 and 2 diabetes mellitus (T1DM and T2DM, respectively) [1,2,3,4]. The clinical examination may confirm the retina’s normality, after a few years of DM some important histological and biochemical lesions usually appear, including adhesion of leukocytes, thickening of the basement membrane as well as loss of pericytes. Advancing dysfunctional process of endothelial cells plays a key role in the structure and pathophysiology of the retina, such as thickening of the basement membrane, loss of perivascular cells, damage to the BRB and neovascularization [14,15]. These alterations are accompanied by important biochemical processes, including formation of advanced glycation end-products, and activation of protein kinase C isoforms and the polyol and hexamine pathways. The decreasing number of pericytes, thickening of the basement membrane, and proliferation of endothelial cells are observed [16,17]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
