Silencing of METTL3 prevents the proliferation, migration, epithelial-mesenchymal transition, and renal fibrosis of high glucose-induced HK2 cells by mediating WISP1 in m6A-dependent manner

• DOI: 10.18632/aging.205401
• Publication Date: 2024-01-29T11:54:19Z
• Authors: Yuanzhen Chen; Ping Li; Mei Lin; Ying Jiang; Guiping Tan; Lianfang Huang; Dan Song

Diabetic nephropathy (DN) is one of the most serious complications in diabetic patients. And m6A modifications mediated by METTL3 are involved multiple biological processes. However, specific function and mechanism DN remains unclear. model mice were first established with streptozotocin, WISP1 expression was confirmed qRT-PCR. Then influences or/and on proliferation, migration, epithelial-mesenchymal transition (EMT) fibrosis-related proteins high glucose (HG)-induced HK2 cells or tested through CCK-8, wound healing, western blot. We revealed that highly expressed renal tissues HG-induced cells. Functionally, silencing could weaken EMT, fibrosis HG-treated cells, overexpression induce Additionally, decrease modification, also notably suppress functions downregulating WISP1. Silencing prevents development process decreasing modification pattern. Therefore, we suggest METTL3/WISP1 axis might be a novel therapeutic target for DN.