Downregulation of AMPK dependent FOXO3 and TFEB involves in the inhibition of autophagy in diabetic cataract

Cataract in diabetic patients is a major cause of blindness in developed and developing countries. The pathogenesis of diabetic cataract development is still not fully understood. Recent basic research studies have emphasized the role of the polyol pathway in the initiation of the disease process. Population-based studies have greatly increased our knowledge concerning the association between diabetes and cataract formation and have defined risk factors for the development of cataract. Diabetic patients also have a higher risk of complications after phacoemulsification cataract surgery compared to nondiabetics. Aldose-reductase inhibitors and antioxidants have been proven beneficial in the prevention or treatment of this sightthreatening condition in in vitro and in vivo experimental studies. This paper provides an overview of the pathogenesis of diabetic cataract, clinical studies investigating the association between diabetes and cataract development, and current treatment of cataract in diabetics.

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Spontaneous resorption of a diabetic cataract in a geriatric dog

Journal of Small Animal Practice ◽

10.1111/j.1748-5827.2005.tb00339.x ◽

2005 ◽

Vol 46 (8) ◽

pp. 406-408 ◽

Cited By ~ 3

Author(s):

E. Gonzalez-Alonso-Alegre ◽

A. Rodriguez-Alvaro

Keyword(s):

Diabetic Cataract

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Lens Lipid Peroxides and Glutathione Concentrations in Diabetic Cataract

Annals of Clinical Biochemistry International Journal of Laboratory Medicine ◽

10.1177/000456329703400211 ◽

1997 ◽

Vol 34 (2) ◽

pp. 190-192 ◽

Cited By ~ 11

Author(s):

D Özmen ◽

I Mutaf ◽

B Özmen ◽

J Mentes ◽

O Bayindir

Keyword(s):

G Protein ◽

Lipid Peroxide ◽

Lipid Peroxides ◽

Thiobarbituric Acid ◽

Thiobarbituric Acid Reactive Substances ◽

Diabetic Cataract ◽

Free Radical Damage ◽

Significant Difference ◽

Radical Damage

This study aims to explore the role of reactive oxygen radicals in the genesis of diabetic cataract. Lipid peroxide (LPO) concentrations in senile ( n = 30) and diabetic ( n = 14) cataractous lenses, were determined as thiobarbituric acid-reactive substances (TBARS) by a method modified from Satoh and Yagi, and reduced glutathione (GSH) concentrations were measured according to Beutler. Lens LPO levels (mean, SD; nmol TBARS/g protein) were significantly higher in diabetics (107·54, 18·12) than senile cataractous subjects (53·54, 15·48) ( P < 0·0001). Lens GSH levels (mean, SD; nmol/g protein) showed no significant difference between diabetics (4·29, 2·05) and senile cataractous subjects (4·68, 3·12). These results suggest that free radical damage is more effective in the genesis of diabetic cataract than in senile cataract.

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