Innovative Center for Aging Research, Yeungnam University Medical Center, Daegu 42415, Korea.
Department of Internal Medicine, Yeungnam Universtiy College of Medicine, Daegu 42415, Korea.
Cells. 2021 Jun 22;10(7):1573. doi: 10.3390/cells10071573.
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.
在 2 型糖尿病中,代谢应激对胰腺β细胞功能和存活(T2D)有负面影响。尽管代谢应激的发病机制很复杂,但氧化还原平衡的失衡会导致异常的组织损伤和β细胞死亡,这是由于β细胞中内源性抗氧化剂表达水平低。在致糖尿病条件下,NADPH 氧化酶引起的β细胞对氧化损伤的易感性与β细胞功能障碍有关。在这里,我们考虑了最近的一些研究进展,即 NADPH 氧化酶如何在糖尿病条件下使氧化还原反应失调,以及 NOX 抑制剂的治疗益处,这可能为理解发病机制和开发旨在治疗或预防与β细胞衰竭相关的代谢应激的策略提供线索。