Retinal Ischemia in Diabetic Retinopathy

Bresnick, George H.; Venecia, Guillermo de; Myers, Frank L.; Harris, Jacob; Davis, Matthew D.

doi:10.1001/archopht.1975.01010020934002

Cited by 143 publications

(94 citation statements)

References 9 publications

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“…Histologic analysis of retinal areas that were nonperfused in vivo has indicated that nonperfused vessels are acellular (1). How the capillary cells die is unclear, but both retinal capillary pericytes and endothelial cells have been found by us to die by a process consistent with apoptosis in humans and animals with diabetes and in experimental galactosemia (another model that develops a diabetic-like retinopathy) (2).…”

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confidence: 99%

Caspase Activation in Retinas of Diabetic and Galactosemic Mice and Diabetic Patients

et al. 2002

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Apoptosis of retinal capillary cells begins early in diabetes and likely contributes to the capillary obliteration that is an important feature of diabetic retinopathy. Caspases are proteolytic enzymes that are closely involved in the induction and execution phases of apoptosis, but their role in the development of diabetic retinopathy has not been studied previously. Our study focused on the measurement of activities of multiple caspases in retinas of mice at different durations of diabetes. Several caspases (including caspases-1, -2, -6, -8, and -9) were activated as early as 2 months of diabetes. The caspases activity pattern changed with increasing duration of disease, suggesting a slowly developing caspases cascade. Activities of executioner caspases (e.g., cas-6 and -3) became elevated after longer duration of diabetes, and the induction of cas-3 activity was associated with the duration of diabetes at which capillary cells begin to show evidence of undergoing apoptosis. Retinas from patients with type 2 diabetes likewise showed a significant increase in activities of cas-1, -3, -4, and -6. For comparison, retinal caspases were also measured in experimental galactosemia, another model that develops a diabetic-like retinopathy. The pattern of caspases activation differed between diabetes and galactosemia, but cas-1 activity became elevated soon after elevation of blood hexose concentration in both. Caspases offer new therapeutic targets to test the role of apoptosis in the development of diabetic retinopathy.

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confidence: 99%

Caspase Activation in Retinas of Diabetic and Galactosemic Mice and Diabetic Patients

et al. 2002

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“…IM can occur with or without macular edema. It causes painless and gradually severe visual loss in color and sharp vision [1][2][3][4][5][6][7][8].…”

Section: Editorialmentioning

confidence: 99%

“…IM is not caused by increased by vascular leakage; it is induced by microvascular blockage and enlargement, with capillary loss and adjacent edema [1][2][3][4][5][6][7][8]. The detection of IM is extremely difficult without the use of fundus angiography.…”

Section: Editorialmentioning

confidence: 99%

“…The detection of IM is extremely difficult without the use of fundus angiography. If the visual loss is not explained ophthalmoscopically or optical coherence tomographically, especially in a diabetic patient, IM is usually responsible for unexplained visual loss, even if the clinical stage of the disease is early or mild [1][2][3][4][5][6][7][8].…”

Section: Editorialmentioning

confidence: 99%

“…Ischaemic maculopathy can occur in retinal arterial or venous occlusion, retinal arteritis, retinopathy of prematurity (ROP), ocular ischemic syndrome, talc retinopathy, proliferative or non-proliferative diabetic retinopathy, pars planitis, Sarcoidosis, cytomegalovirus retinitis caused by AIDS, familial exudative vitreoretinopathy, Eales' disease involving the macula [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Additionally, it has been reported that it can be developed following intravitreal antivascular endothelial growth factor injection [21,22].…”

Section: Editorialmentioning

confidence: 99%

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