Fig. 8.

Summary of the proposed mechanism in renal tubular epithelial cells in obesity and metabolic syndrome. An increased FA load on albumin presents increased FA load to the mitochondrial β-oxidation cycle after endocytosis. This, together with other cellular sources, will increase peroxide production and exhaust cytosolic Prdx2 defense by overoxidation. Increased peroxide levels will activate the redox-sensitive pJNK/caspase-3 apoptotic pathway leading to cell death. Blocking mitochondrial FA entry with etomoxir or overexpressing Prdx2 will provide defense against the activation of the redox-sensitive apoptotic pathway.