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Published on: January 12, 2024
Dicarbonyl Stress Mimics Diabetic Neurovascular Damage in the Retina
M Kolibabka1, P Friedrichs1, N Dietrich1
15th Medical Department, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
Abstract:
The net effect of euglycemic treatment is grossly overestimated in diabetes mellitus and retinopathy, similar to what is observed in diabetic individuals, is found in the absence of chronic hyperglycemia. Explanations of this clinical paradox include the excess generation of reactive intermediates of metabolism. Excess formation or impaired detoxification of reactive intermediates can also result in multiple posttranslational modifications with a wide range of cellular dysfunctions. The multicellular neurovascular unit represents the response element of the retina which is crucial for the development of diabetic retinopathy. Current evidence suggests that increased reactive intermediates in the retina induce (micro-)glial activation, neurodegeneration and vasoregression similar to alterations found in the diabetic retina. Reactive metabolites can be lowered by metabolic signal blockade, by an activation of detoxification pathways and by quenching. The translation of these novel findings into treatment of patients with complications is important to reduce individual suffering and financial burden for societies.Quick Summary:Increased levels of reactive intermediates, independent of blood glucose levels, are linked to damage of the neurovascular unit of the diabetic retina.
Insights
Reactive intermediates, not just high blood sugar, damage the diabetic retina's neurovascular unit. Lowering these metabolites may offer new therapeutic strategies for diabetic retinopathy.
Area of Science:
- Biochemistry
- Ophthalmology
- Metabolic Disorders
Background:
- Euglycemic treatment effects in diabetes mellitus and retinopathy are often overestimated.
- Diabetic retinopathy development involves the neurovascular unit in the retina.
Purpose of the Study:
- To investigate the role of reactive intermediates in diabetic retinopathy, independent of hyperglycemia.
- To explore potential therapeutic strategies targeting reactive metabolites.
Main Methods:
- Analysis of reactive intermediate generation and detoxification in the retina.
- Assessment of posttranslational modifications and cellular dysfunction.
- Evaluation of (micro-)glial activation, neurodegeneration, and vasoregression.
Main Results:
- Increased reactive intermediates, independent of chronic hyperglycemia, contribute to diabetic retinopathy.
- Excess reactive metabolites cause neurovascular unit damage, including (micro-)glial activation and vasoregression.
- Reactive metabolites can be reduced through metabolic signal blockade, enhanced detoxification, or quenching.
Conclusions:
- Reactive intermediates are a key driver of diabetic retinopathy pathology.
- Targeting reactive metabolite pathways offers a novel therapeutic avenue for diabetic complications.
- Reducing patient suffering and societal costs associated with diabetic retinopathy is a critical goal.
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