It also downregulated the expression of inflammatory,fibrotic, and EMT-related proteins, including IL-1β, IL-6, TNF-α,TGF-β, phospho-Smad2/3, collagen 1, α-SMA, and vimentinin mouse kidney tissues through 21 days after the induction of AKI.On the other hand, diosgenin protected human renal tubular epithelialcells from in vitro hypoxia injury that mimic in vivo I/R by decreasingoxidative stress and inflammatory, fibrotic, EMT, and apoptotic proteinexpression through the NOX4/p65 signaling pathway. The gene discussed is NOX4; the disease is acute kidney injury.