March 25, 2020Open Access

AKR1B1-Induced Epithelial–Mesenchymal Transition Mediated by RAGE-Oxidative Stress in Diabetic Cataract Lens

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Abstract

Our results suggest that AKR1B1 overexpression can decrease AMPK activation, thereby increasing AcSOD2 and RAGE-induced EMT in epithelial human lens of DM cataracts. These novel findings suggest that AKR inhibitors may be candidates for the pharmacological prevention of cataracts in patients with DM.

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Authors

Tsung‐Tien Wu

Yingying Chen

Hui-Yu Chang

Journals

SHILAP Revista de lepidopterología

Antioxidants

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Institutions

National Yang Ming Chiao Tung University

National Sun Yat-sen University

Kaohsiung Veterans General Hospital

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AKR1B1-Induced Epithelial–Mesenchymal Transition Mediated by RAGE-Oxidative Stress in Diabetic Cataract Lens

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Abstract

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