In diabetes, hyperglycemia causes the excessive generation of advanced glycation end products (AGEs) in renal tissue and then results in the accumulation of extracellular matrix (ECM) and the release of profibrotic cytokines, such as transforming growth factor β1 (TGF-β1), connective tissue growth factor (CTGF), and the angiogenic growth factor (VEGF), which ultimately leads to renal fibrosis and inflammation [8]. Here, CCN2 is linked to renal fibrosis.