In summary, we demonstrated that MALAT1 promoted the interaction of LIN28A and Nox4 to stabilize Nox4 stability and activating the AMPK/mTOR signaling, thus aggravating HG-induced renal tubular epithelial cell injury in DN, which identified a novel MALAT1/LIN28A/Nox4 axis in DN progression (Figure 10). This evidence concerns the gene LIN28A and liver dysplastic nodule.