Much of the effort to understand diabetic retinopathy has focused on vascular pathology. Due to the influence of diabetes on systemic physiology, it is thought that many changes in retinal vascular cells likely stem from direct biochemical disruptions such as hyperglycemia. Other contributing factors may include circulating cytokines, advanced glycation end products, cholesterol, albumin, and electrolytes, and more complex functional changes such as reduced elasticity in erythrocytes and other blood cells. These and other changes could be responsible for generating the vascular pathologies that have been well established in diabetic retinopathy. There is increasing evidence, however, for involvement of the neural elements of the retina, the neurons and glial cells, and it is no longer clear if the pathological changes in these cells result from vascular dysfunction, such as the reduction in effectiveness of the blood-retinal barrier, or if diabetic physiology induces neural pathology, which in turn gives rise to vascular changes. A third possibility is that early vascular and neural responses to diabetes are independent phenomena that are triggered by different factors.
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