| Autor: |
Elumalai S; Innovative Center for Aging Research, Yeungnam University Medical Center, Daegu 42415, Korea., Karunakaran U; Innovative Center for Aging Research, Yeungnam University Medical Center, Daegu 42415, Korea., Moon JS; Innovative Center for Aging Research, Yeungnam University Medical Center, Daegu 42415, Korea.; Department of Internal Medicine, Yeungnam Universtiy College of Medicine, Daegu 42415, Korea., Won KC; Innovative Center for Aging Research, Yeungnam University Medical Center, Daegu 42415, Korea.; Department of Internal Medicine, Yeungnam Universtiy College of Medicine, Daegu 42415, Korea. |
| Abstrakt: |
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. |
