ASH2L Aggravates Fibrosis and Inflammation through HIPK2 in High Glucose-Induced Glomerular Mesangial Cells.

ABSTRACT: Diabetic nephropathy (DN) is a leading cause of end-stage renal disease and continues to be a threat to patients with diabetes. Dysfunction of glomerular mesangial cells (GMCs) is the main contributing factor to glomerulosclerosis, which is a pathological feature of DN. The epigenetic factor ASH2L has long been thought to be a transcriptional activator, but its function and involvement in diabetic nephropathy is still unclear. Here, we investigated the effect of ASH2L on the regulation of fibrosis and inflammation induced by high glucose in mouse mesangial cells (mMCs). We observed that ASH2L expression is increased in high glucose-induced mMCs, while loss of ASH2L alleviated fibrosis and inflammation. Furthermore, ASH2L-mediates H3K4me3 of the homeodomain-interacting protein kinase 2 (HIP

SUBMITTER: Zhong W 

PROVIDER: S-EPMC9816940 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature