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Published on: June 25, 2018
NADPH Oxidase (NOX) Targeting in Diabetes: A Special Emphasis on Pancreatic β-Cell Dysfunction
Suma Elumalai1, Udayakumar Karunakaran1, Jun-Sung Moon1,2
1Innovative Center for Aging Research, Yeungnam University Medical Center, Daegu 42415, Korea.
Abstract:
In type 2 diabetes, metabolic stress has a negative impact on pancreatic β-cell function and survival (T2D). Although the pathogenesis of metabolic stress is complex, an imbalance in redox homeostasis causes abnormal tissue damage and β-cell death due to low endogenous antioxidant expression levels in β-cells. Under diabetogenic conditions, the susceptibility of β-cells to oxidative damage by NADPH oxidase has been related to contributing to β-cell dysfunction. Here, we consider recent insights into how the redox response becomes deregulated under diabetic conditions by NADPH oxidase, as well as the therapeutic benefits of NOX inhibitors, which may provide clues for understanding the pathomechanisms and developing strategies aimed at the treatment or prevention of metabolic stress associated with β-cell failure.
Insights
Type 2 diabetes impairs pancreatic beta-cell function due to redox imbalance. NADPH oxidase contributes to oxidative damage, suggesting NOX inhibitors as a therapeutic strategy for beta-cell failure.
Area of Science:
- Endocrinology
- Metabolic Disease Research
- Cell Biology
Background:
- Type 2 diabetes (T2D) involves metabolic stress negatively impacting pancreatic beta-cell function and survival.
- Redox homeostasis imbalance and reduced endogenous antioxidants in beta-cells lead to oxidative damage and cell death.
- NADPH oxidase activity is implicated in beta-cell dysfunction under diabetogenic conditions.
Purpose of the Study:
- To review recent insights into redox response deregulation in T2D.
- To explore the role of NADPH oxidase in beta-cell failure.
- To discuss the therapeutic potential of NOX inhibitors for T2D-associated metabolic stress.
Main Methods:
- Literature review of studies on redox homeostasis in type 2 diabetes.
- Analysis of the role of NADPH oxidase in beta-cell pathophysiology.
- Evaluation of preclinical and clinical data on NOX inhibitors.
Main Results:
- Diabetic conditions deregulate the cellular redox response, primarily through NADPH oxidase.
- Oxidative stress induced by NADPH oxidase contributes significantly to beta-cell dysfunction and apoptosis.
- NOX inhibitors show promise in preclinical models for protecting beta-cells.
Conclusions:
- Understanding NADPH oxidase-mediated redox imbalance is crucial for T2D pathogenesis.
- NOX inhibitors represent a potential therapeutic avenue for preventing or treating beta-cell failure in type 2 diabetes.
- Targeting redox pathways may offer novel strategies for metabolic stress management in diabetes.
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