Mettl3-Mediated m6A Modification Represents a Novel Therapeutic Target for FSGS.

ABSTRACT: Focal segmental glomerulosclerosis (FSGS) is a common glomerular lesion that manifests as a primary podocyte injury. Multiple genetic risk factors have been reported to be associated with the development of FSGS. However, whether epigenetic factors, especially N6-methyladenosine (m6A) modifications, are involved in the pathogenesis of FSGS remains unclear. By generating a mouse line with a specific deletion of N6-adenosine-methyltransferase-like 3 (Mettl3) in podocytes (Mettl3^podkomice), podocytes are isolated and performed RNA-seq. It is shown that RNA m6A methylation levels are reduced in the renal glomeruli of both animal models and patients with FSGS. A significant decrease in RNA m6A levels in podocytes and the development of an FSGS phenotype are observed in the Mettl3

SUBMITTER: Zhu F 

PROVIDER: S-EPMC12915192 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature