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By contrast, preclinical in vivo and in vitro studies both indicate that incretin receptor agonism can attenuate fibrogenic signalling in models of kidney disorders, and thus the positive clinical trial data on kidney function outcome measures may, in part, be mediated by inhibition of fibrosis

[19] presented the direct confirmation of Nrf2s crucial function in protecting against T2DM-induced DCM using sulforaphane (SFN)