被撤回的出版物: LncRNA MALAT1/microRNA let-7f/KLF5 axis regulates podocyte injury in diabetic nephropathy (Retracted article. See vol. 318, 2023)

Objective: The abnormal expression of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) has been demonstrated to exert pivotal effects in human diseases. We focused on the functions of metastasis associated lung adenocarcinoma transcript 1 (MALAT1) and microRNA let-7f on diabetic nephropathy (DN). Methods: The diabetes (db/db) mice were treated with silenced MALAT1, then the baseline indicators, pathology changes, marker proteins of podocyte injury (nephrin, podocin, desmin and Cleaved caspase-3), oxidative stress indicators and inflammatory factors in renal tissues were determined. Murine podocyte MPC5 cells were stimulated by high glucose (HG) and transfected with sh-MALAT1 or let-7f mimic, then the cell migration, adhesion ability and apoptosis were evaluated. Moreover, the binding relationship between MALAT1 and let-7f, and the targeting relationship between let-7f and kruppel-like factor 5 (KLF5) were confirmed. Results: Silenced MALAT1 could improve baseline indicators of DN mice, and also improved pathology, increased nephrin and podocin expression, decreased desmin and Cleaved caspase-3 expression, and restrained oxidative stress and inflammatory reaction in their renal tissues. Additionally, elevated let-7f and reduced MALAT1 could restrict migration and apoptosis of HG-induced MPC5 cells, and promoted the cell adhesion ability. Conclusion: Results in our research indicated that the reduced MALAT1 could relieve the podocyte injury in DN by upregulating let-7f and inhibiting KLF5, which may be helpful for DN therapy.

Automated summary

The research findings suggest that reducing MALAT1 can improve baseline indicators and pathology changes in diabetic nephropathy mice, while also inhibiting oxidative stress and inflammatory reaction in renal tissues. Furthermore, upregulation of let-7f and downregulation of MALAT1 can restrict migration and apoptosis of MPC5 cells induced by high glucose, and enhance cell adhesion ability.