Advanced Glycation End Products Mediate Epigenetic Alteration of H3K27me3 in Renal Proximal Tubular Cells: Potential Role in Metabolic Memory.

ABSTRACT: The accumulation of advanced glycation end products (AGEs) is a hallmark of prolonged high glucose levels in diabetes mellitus. We have previously reported that hypoxia and AGEs cause epigenetic modification of the repressive mark H3K27me3 in podocytes by downregulation of enhancer of zeste homolog 2 (EZH2) and nuclear inhibitor of protein phosphatase 1 (NIPP1). However, their impact on proximal tubular cells remains unclear. The aim of this study was to investigate the role of AGEs and diabetes on the epigenetic modifications of EZH2 and H3K27me3 in proximal tubular cells and in diabetic (db/db) mice. Our results show that AGEs reduced EZH2 expression in TKPTS cells, thereby decreasing the tri-methylation of H3K27. qRT-PCR analysis revealed upregulation of genes known to contribute

SUBMITTER: Ludewig L 

PROVIDER: S-EPMC12607550 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature