This increases ROS production and the activation of protein kinase C (PKC), nuclear factor-kappa B (NF-κB), inhibitor of NF-κB kinase subunit beta (IKKβ), c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and mammalian target of rapamycin (mTOR), leading to lipid accumulation, hypertrophy, glomerulosclerosis, and apoptosis, resulting in a decline in GFR (Figure 2) [34,40,48,50]. Here, MTOR is linked to glomerulosclerosis.