LncRNA MALAT1 Aggravates Renal Tubular Injury via Activating LIN28A and the Nox4/AMPK/mTOR Signaling Axis in Diabetic Nephropathy

• DOI: 10.3389/fendo.2022.895360
• Publication Date: 2022-06-23T05:16:28Z
• Authors: Panai Song; Yinyin Chen; Zhiwen Liu; Hong Liu; Li Xiao; Lin Sun; Jiali Wei; Liyu He
• Keywords: NOX4; Renal Injury; MALAT1

Background Diabetic nephropathy (DN) is a serious complication among patients with diabetes. Elucidating its pathogenesis crucial for identifying novel biomarkers and therapeutic targets DN. Methods DN tissues were harvested examining MALAT1, LIN28A Nox4. Human kidney-2 (HK-2) cells treated high glucose (HG) establishing cell model of Cell viability was examined by MTT assay. HG-induced apoptosis secretion TNF-α IL-6 analyzed TUNEL ELISA assays, respectively. RIP RNA pull-down assays applied to analyze the interaction between Nox4 in HK-2 human embryonic kidney 293T (HEK-293T) cells. A rat established determine role MALAT1 vivo . Results upregulated HG-treated Overexpression or reduced enhanced apoptosis, ROS generation inflammatory cytokines cells, whereas knockdown exerted opposite effects. Furthermore, directly interacted LIN28A. Moreover, facilitated increase stability. Knockdown relieved injury suppressing AMPK/mTOR signaling alleviated renal tubular epithelial Nox4/AMPK/TOR Conclusion activates via interacting stabilize mRNA, thereby aggravating glucose-induced injury. Our findings provide potential