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Ferroptosis and kidney diseases

  • Nephrology - Review
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Abstract

Ferroptosis is a form of iron-dependent, non-apoptotic regulated cell death, which is characterized by the accumulation of lipid hydroperoxides to lethal levels. Ferroptosis recently has been shown to have implications in diverse kidney diseases, such as acute kidney injury, polycystic kidney disease and renal cell carcinoma. This review summarizes current research on ferroptosis, its underlying mechanisms and its role in the progression of different kidney diseases to provide more information regarding treatment and prevention of these destructive diseases.

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Fig. 1

Free iron can interact with ROS, forming a radical and rapid reacts with oxygen to generate a lipid peroxide via the Fenton reaction. Thus, iron import, export, storage, and turnover impact ferroptosis sensitivity. Lipid peroxides and their degradation products are controlled by GSH-based redox reactions. System xc−imports cystine, which is reduced to cysteine and used to synthesize glutathione. GPX4 reduces membrane phospholipid hydroperoxides to suppress ferroptosis. Downstream of NRF2 participated in many ferroptotic process maintaining redox homeostasis, iron/heme metabolism and lipid metabolism

Fig. 2

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  1. Department of Nephrology, Central South University, Xiangya Hospital, Xiangya Road No 87, Changsha, Hunan, 41008, China

    Shumei Tang & Xiangcheng Xiao

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Tang, S., Xiao, X. Ferroptosis and kidney diseases. Int Urol Nephrol 52, 497–503 (2020). https://doi.org/10.1007/s11255-019-02335-7

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