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Ferroptosis Signaling in Pancreatic β-Cells: Novel Insights & Therapeutic Targeting

Journal

Publisher

MDPI
DOI: 10.3390/ijms232213679

Keywords

iron; NADPH oxidase; oxidative stress; diabetes; reactive oxygen species; ferroptosis

Funding

  1. National Research Foundation of Korea (NRF) - Korean government [NRF-2020R1A2C1003649, NRF2020R1A2C4002626]

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Metabolic stress impairs pancreatic beta-cell survival and function, which is associated with the imbalance in redox equilibrium and ferroptotic-like malfunction in beta-cells.
Metabolic stress impairs pancreatic beta-cell survival and function in diabetes. Although the pathophysiology of metabolic stress is complex, aberrant tissue damage and beta-cell death are brought on by an imbalance in redox equilibrium due to insufficient levels of endogenous antioxidant expression in beta-cells. The vulnerability of beta-cells to oxidative damage caused by iron accumulation has been linked to contributory beta-cell ferroptotic-like malfunction under diabetogenic settings. Here, we take into account recent findings on how iron metabolism contributes to the deregulation of the redox response in diabetic conditions as well as the ferroptotic-like malfunction in the pancreatic beta-cells, which may offer insights for deciphering the pathomechanisms and formulating plans for the treatment or prevention of metabolic stress brought on by beta-cell failure.

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