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Fig. 8 | Molecular Medicine

Fig. 8

From: IκB kinase promotes Nrf2 ubiquitination and degradation by phosphorylating cylindromatosis, aggravating oxidative stress injury in obesity-related nephropathy

Fig. 8

Schematic representation of the proposed mechanism by which the phosphorylation of IKK and CYLD mediated the activation of the Nrf2/ARE pathway, thereby inducing oxidative stress in human kidney cells. The imbalance between the increase in ROS and/or the decrease in antioxidant activity promotes oxidative stress injury to tissues or cells. Regulation of mitochondrial production of ROS is required for the proper adaptation of renal cells to metabolic stress. The phosphorylation of IKK induced phosphorylation of CYLD results in the inactivation of its deubiquitination activity and is thus unable to prevent the ubiquitination of Nrf2, which promoted the production of ROS and the depolarization of mitochondrial membrane potential and ultimately facilitated oxidative stress injury in vitro, which is conducive to the development of ORN

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