CCL2 and liver dysplastic nodule: Its probable mechanism includes activation of renal AGE-RAGE signaling pathways, decreasing levels of monocyte chemotactic protein-1 (MCP-1) and PKC-A, which consequently reduces the production of slit diaphragm proteins such as nephrin and podocin, thereby mitigating the impact of AGE-mediated DN pathogenesis (Muthenna et al., 2014).