Abnormal expression of these cytokines may activate renal fibrosis-related signaling pathways, induce EndMT/EMT/MMT, and promote the accumulation of ECM, which ultimately stimulates the expression of fibrosis-related proteins (e.g. α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF)) and glomerulosclerosis (42–47). Here, CCN2 is linked to renal fibrosis.