| Autor: |
Crawford TN; Charleston Neuroscience Institute, Retina Division, Charleston, SC 29412, USA. crawfordtalia@yahoo.com, Alfaro DV 3rd, Kerrison JB, Jablon EP |
| Jazyk: |
angličtina |
| Zdroj: |
Current diabetes reviews [Curr Diabetes Rev] 2009 Feb; Vol. 5 (1), pp. 8-13. |
| DOI: |
10.2174/157339909787314149 |
| Abstrakt: |
Diabetic retinopathy, a secondary microvascular complication of diabetes mellitus is the leading cause of blindness in the Unites States amongst individuals age 20 to 64. Two major retinal problems cause most of the diabetes-related vision loss: diabetic macular edema and complications from abnormal retinal blood vessel growth, angiogenesis. Secondary to angiogenesis, increased retinal blood flow is of pathogenic importance in the progression of diabetic retinopathy. Understanding the role of hyperglycemia seems to be the most critical factor in regulating retinal blood flow, as increased levels of blood glucose are thought to have a structural and physiological effect on retinal capillaries causing them to be both functionally and anatomically incompetent. High blood glucose induces hypoxia in retinal tissues, thus leading to the production of VEGF-A (vascular endothelial growth factor protein). Hypoxia is a key regulator of VEGF-induced ocular neovascularization. Secondary to the induction of VEGF by hypoxia, angiogenesis can be controlled by angiogenic inducers and inhibitors. The balance between VEGF and angiogenic inhibitors may determine the proliferation of angiogenesis in diabetic retinopathy. Since VEGF-A is a powerful angiogenic inducer, utilizing anti-VEGF treatments has proved to be a successful protocol in the treatment of proliferative diabetic retinopathy. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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