Redox status is a key determinant in the fate of every cell, β-cell in particular.  β-cells are not primarily detoxifying like e.g. hepatocytes or kidney cells and thus do not possess extensive antioxidant defense machinery. However, they show a wide range of redox regulating proteins, such as peroxiredoxins, thioredoxins or thioredoxin reductases, etc., being functionally compartmentalized. These proteins keep fragile redox homeostasis and serve as messengers and amplifiers of redox signaling which is inevitable for proper β-cell function (particularly insulin secretion) and maintenance. Dysbalance in redox homeostasis establishes oxidative stress which accompanies the development of type 2 diabetes.

Redox status is a key determinant in the fate of every cell, β-cell in particular.  β-cells are not primarily detoxifying like e.g. hepatocytes or kidney cells and thus do not possess extensive antioxidant defense machinery. However, they show a wide range of redox regulating proteins, such as peroxiredoxins, thioredoxins or thioredoxin reductases, etc., being functionally compartmentalized. These proteins keep fragile redox homeostasis and serve as messengers and amplifiers of redox signaling which is inevitable for proper β-cell function and maintanance.