| Literature DB >> 34206537 |
Suma Elumalai1, Udayakumar Karunakaran1, Jun-Sung Moon1,2, Kyu-Chang Won1,2.
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.Entities:
Keywords: NADPH oxidase; diabetes mellitus; insulin-secreting cells; oxidative stress; reactive oxygen species
Year: 2021 PMID: 34206537 DOI: 10.3390/cells10071573
Source DB: PubMed Journal: Cells ISSN: 2073-4409 Impact factor: 6.600