Metformin inhibits high glucose‐induced apoptosis of renal podocyte through regulating miR‐34a/SIRT1 axis

• DOI: 10.1002/iid3.1053
• Publication Date: 2024-01-19T11:50:37Z
• Authors: Xudong Zhuang; Zhuye Sun; Huasheng Du; Tianhui Zhou; Jing Zou; Wei Fu
• Keywords: Viability assay

Abstract Background Previous studies have reported SIRT1 was inversely modulated by miR‐34a, However, mechanism of metformin (MFN)'s renal podocyte protection under high glucose (HG) conditions and the connection between miR‐34a expression in diabetic nephropathy (DN) remain unclear. Method We aimed to further elucidate role HG‐treated podocytes DN. A conditionally immortalized human cell line cultivated d ‐glucose (30 mM). Results Microarray RT‐qPCR revealed that downregulated podocytes. Additionally, levels increased MFN‐treated HG‐induced CCK‐8 assay, colony formation flow cytometry, Western blot detection showed HG treatment reduced viability promoted via treatment, MFN reversed this phenotypic change. MiR‐34a upregulation caused restored suppressed apoptosis podocytes, downregulation led damaged survival induced MFN‐administered The dual luciferase reporter assay 3′‐UTR a direct target. Further demonstrated an elevation HG‐exposed whereas decreased levels. In addition, expression, inhibition cells. MFN‐induced suppresses acting on SIRT1. Conclusion This study proposes promising approach interpret mechanisms action MFN‐miR‐34a axis involved