Prediction of diabetic retinopathy: Role of oxidative stress and relevance of apoptotic biomarkers

被引:46
作者
Al-Shabrawey M. [1 ,2 ,3 ]
Smith S. [2 ,4 ]
机构
[1] Oral Biology and Anatomy, School of Dentistry, Medical College of Georgia, Augusta
[2] Ophthalmology and Vision Discovery Institute, Medical College of Georgia, Augusta
[3] Opthalmology, King Saud University, Riyadh
[4] Cellular Biology and Anatomy, Medical College of Georgia, Augusta
基金
美国国家卫生研究院;
关键词
Apoptosis; Biomarkers; Diabetic retinopathy; Oxidative stress;
D O I
10.1007/s13167-010-0002-9
中图分类号
学科分类号
摘要
Diabetic retinopathy (DR) is the foremost cause of blindness in working-aged worldwide; it is characterized by vascular and neuronal degeneration. Features of DR include leukocyte adhesion, increased vascular permeability, neovascularization and neuronal cell death. Early diagnosis and intervention are important to prevent or at least ameliorate the development of DR. Recent reports indicate that pathophysiological mechanisms leading to diabetic retinopathy include oxidative stress and retinal cell death cascades. Circulating biomarkers of oxidative stress such as malondialdehyde (MDA), thiobarbituric acid reacting substances (TBARS), conjugated diene (CD), advanced oxidation protein products (AOPP), protein carbonyl, 8- hydroxydeoxyguanosin (8-OHdG), nitrotyrosine, and F(2) isoprostanes and pro-apoptosis molecules (caspase-3, Fas, and Bax) are associated with increased susceptibility to develop DR in diabetic subjects. Thus, identification of oxidative stress and cell death biomarkers in diabetic patients could be in favor of predicting, diagnosis, and prevention of DR, and to target for novel therapeutic interventions. © European Association for Predictive, Preventive and Personalised Medicine 2010.
引用
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页码:56 / 72
页数:16
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共 179 条
  • [1] Kowluru R.A., Tang J., Kern T.S., Abnormalities of retinal metabolism in diabetes and experimental galactosemia. Vii. Effect of long-term administration of antioxidants on the development of retinopathy, Diabetes, 50, pp. 1938-1942, (2001)
  • [2] Brownlee M., Biochemistry and molecular cell biology of diabetic complications, Nature, 414, pp. 813-820, (2001)
  • [3] Kowluru R.A., Abbas S.N., Diabetes-induced mitochondrial dysfunction in the retina, Invest Ophthalmol Vis Sci, 44, pp. 5234-5327, (2003)
  • [4] Giardino I., Fard A.K., Hatchell D.L., Et al., Aminoguanidine inhibits reactive oxygen species formation, lipid peroxidation, and oxidant-induced apoptosis, Diabetes, 47, pp. 1114-1120, (1998)
  • [5] Barber A.J., A new view of diabetic retinopathy: A neurodegenerative disease of the eye, Prog Neuropsychopharmacol Biol Psychiatry, 27, pp. 283-290, (2003)
  • [6] Antonetti D.A., Barber A.J., Bronson S.K., Et al., Diabetic retinopathy: Seeing beyond glucose-induced microvascular disease, Diabetes, 55, pp. 2401-2411, (2006)
  • [7] Smith S., The impact of diabetes on neuronal, glial and vascular cells of the retina: Implications for the pathogenesis of diabetic retinopathy, Retinal Degenerations: Biology, Diagnostics, and Therapeutics, (2007)
  • [8] Bresnick G.H., Korth K., Groo A., Et al., Electroretinographic oscillatory potentials predict progression of diabetic retinopathy. Preliminary report, Arch Ophthalmol, 102, pp. 1307-1311, (1984)
  • [9] de Faria L.J.M., Katsumi O., Cagliero E., Et al., Neurovisual abnormalities preceding the retinopathy in patients with longterm type 1 diabetes mellitus, Graefes Arch Clin Exp Ophthalmol, 239, pp. 643-648, (2001)
  • [10] Mizutani M., Kern T.S., Lorenzi M., Accelerated death of retinal microvascular cells in human and experimental diabetic retinopathy, J Clin Invest, 97, pp. 2883-2890, (1996)