Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P06889 (
Mol
)
630,302
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Diabetic nephropathy (DN), a serious complication of hyperglycemia, is one of the most common causes of end-stage renal disease (ESRD). Glomerular podocyte injury is a major mechanism that leads to DN. However, the mechanisms underlying podocyte injury are ambiguous. In this study, we sought to investigate the contribution of
SET domain-containing protein 6
(
SETD6
) to the pathogenesis of podocyte injury induced by glucose (GLU) and palmitic acid (PA), as well as the underlying mechanisms. Our results showed that GLU and PA treatment significantly decreased
SETD6
expression in mouse podocytes. Besides, Cell Counting Kit-8 (CCK-8) and flow cytometry assay demonstrated that silencing of
SETD6
silence obviously enhanced cell viability, and suppressed apoptosis in GLU and PA-induced podocytes. We also discovered that downregulation of
SETD6
suppressed GLU and PA-induced ROS generation and podocyte mitochondrial dysfunction. Nrf2-Keap1 signaling pathway was involved in the effect of
SETD6
on mitochondrial dysfunction. Taken together, silencing of
SETD6
protected mouse podocyte against apoptosis and mitochondrial dysfunction through activating Nrf2-Keap1 signaling pathway. Therefore these data provide new insights into new potential therapeutic targets for DN treatment.
J
Mol
Histol 2020 Oct
PMID:Down-regulation of SETD6 protects podocyte against high glucose and palmitic acid-induced apoptosis, and mitochondrial dysfunction via activating Nrf2-Keap1 signaling pathway in diabetic nephropathy. 3280 70
