SMAD3 and liver dysplastic nodule: also found that circ_TAOK1 was greatly elevated in exosomes secreted by HG-treated GMCs and serum exosomes from DN patients, with significant up-regulation of the levels of PCNA, cytokinin D1, α-SMA, FN, N-cadherin, and SMAD3 and significant down-regulation of the level of E-cadherin, which promoted the proliferation, fibrosis, accelerated fibrosis and EMT, while KO-circTAOK1 reversed the above effects, suggesting that exosomal circ_TAOK1 promotes GMC injury (137).