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Related Experiment Video

Updated: Apr 19, 2026

Characterization of Molecular Mechanisms of In vivo UVR Induced Cataract

Characterization of Molecular Mechanisms of In vivo UVR Induced Cataract

Published on: November 28, 2012

Aldose reductase expression as a risk factor for cataract.

Anson Snow¹, Biehuoy Shieh¹, Kun-Che Chang¹

¹Department of Ophthalmology, University of Colorado Denver, CO, USA.

Chemico-Biological Interactions

|December 27, 2014

Summary

High aldose reductase (AR) gene expression may increase the risk of diabetic eye disease. Overexpression of AR in mice led to cataract formation and altered cell signaling pathways, suggesting a link between AR levels and diabetic complications.

Keywords:

AKR1B1 Aldose reductase Cataract Diabetes

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Induction and Analysis of Oxidative Stress in Sleeping Beauty Transposon-Transfected Human Retinal Pigment Epithelial Cells

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A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

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Published on: July 14, 2016

Area of Science:

Biochemistry
Ophthalmology
Genetics

Background:

Diabetic eye diseases like cataracts and retinopathy are linked to aldose reductase (AR).
Individual susceptibility to diabetic eye complications varies, suggesting other risk factors are involved.
Elevated AR gene expression is hypothesized to increase the risk of developing these complications.

Purpose of the Study:

To investigate the hypothesis that elevated AR gene expression confers a higher risk for diabetic eye disease.
To examine the onset and severity of diabetes-induced cataract in transgenic mice with varying levels of human AR transgene expression.

Main Methods:

Utilized transgenic mice (AR-TG) engineered to overexpress the human AR (AKR1B1) gene.
Induced experimental diabetes in AR-TG mice (homozygous and heterozygous) and compared them to non-transgenic controls.
Assessed lens structural changes, sorbitol levels, and signaling pathways (ERK1/2, JNK1/2) in response to diabetes and AR overexpression.

Main Results:

Homozygous AR-TG mice developed cataracts and lens vacuoles specifically after diabetes induction.
Nondiabetic AR-TG mice showed high lenticular sorbitol levels without structural changes.
AR overexpression increased activated ERK1/2 and JNK1/2; diabetes induction decreased these signaling molecules in AR-TG mice.

Conclusions:

High AR expression, in conjunction with hyperglycemia and insulin deficiency, may predispose the lens to cataract formation.
Disturbances in ERK and JNK signaling pathways due to AR overexpression can disrupt the balance of cell growth and apoptosis in the lens.
AR may be a significant risk factor for diabetic eye disease, influencing lens homeostasis and transparency.