It has been shown that in the early stage, BM-MSCs circulating to the kidney and RR-MSCs can still secrete IDO and other immunomodulatory factors to resist the process of renal fibrosis mediated by small doses of TGF-β1; when the injury continues to worsen and the microenvironmental inflammation increases and exceeds the regulatory capacity of MSCs, a large number of MSCs will differentiate into myofibroblasts under the stimulation of large amounts of TGF-β1 and other pro-fibrotic factors [15,16,41] (Figure 2). Here, TGFB1 is linked to renal fibrosis.