Fig. 2

Schematic representation of the mitochondrial involvement in chronic kidney disease (CKD). In this pathological condition, mitochondrial impairment (mainly characterized by a reduction in mitochondrial biogenesis, loss of mitochondrial membrane potential, and drop of ATP production) causes a great release of ROS that could contribute to chronic microinflammation through NLRP3 inflammasome activation. At the same time, during CKD, nuclear factor erythroid 2-related factor 2 (NRF-2) and one of its target gene superoxide dismutase 2 (SOD2) are up-regulated by oxidative stress, in the attempt to neutralize ROS production. Notably, this effect has been observed by our group [54] in PBMCs