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Summary of the proposed role of BAI on STZ-induced DN. BAI, and particularly the kidney-targeted BAI-LZM conjugate, produced inhibition of renal fibrosis and inflammation via the NF-κB, TGF-β1/Smad3 and IGF-1/p38 MAPK signaling pathways. BAI and BAI-LZM can harness the body’s cytoprotective pathways to reactivate autophagy (autophagy markers, mTOR and SIRT1) to ameliorate DN outcomes
