Diabetic retinopathy is a major cause of blindness. Underlying pathogenicmechanisms that have been suggested include the non-enzymatic glycosylation pathwayand production of advanced glycation end-products (AGEs), retinal neurodegeneration and inflammation, and enhanced reactive oxygen species (ROS) generation. Here, theauthors discuss how the UV component of solar radiation may potentially enhance theprogression of diabetic retinopathy. The mechanisms we suggest are: (1) In hightemperatureenvironments with intense solar radiation, the amount of UV reaching theretina is sufficient to increase de novo ROS generation. (2) Under UV-A irradiation,AGEs generate ROS. (3) Enhanced oxidative stress promotes generation of AGEs. (4)UV-B may enhance intraocular inflammation (production of endothelin and IL-6)in DR patients, and this in turn may accelerate AGE generation. (5) UV-B and ROSindependently up-regulate VEGF expression, inducing fibrovascular proliferation andinflammation. (6) ROS induce apoptosis of the retinal neurons and pericytes. (7)Oxidation of the glycated proteins and lipids produces potentially toxic substanceswithin the retina. Thus, UV irradiation could enhance the progression of diabeticretinopathy, so strategies to limit UV exposure such as wearing protective sunglasses orusing photochromic lenses that could attenuate this progression will become increasinglyimportant as humans are exposed to greater levels of solar radiation.
|Original language||English (US)|
|Title of host publication||Hypotheses in Clinical Medicine|
|Publisher||Nova Science Publishers, Inc.|
|Number of pages||7|
|State||Published - Dec 1 2013|
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