Set7 Methyltransferase and Phenotypic Switch in Diabetic Glomerular Endothelial Cells

Maxwell S
April 17, 2024
J Am Soc Nephrol
https://pubmed.ncbi.nlm.nih.gov/38630537

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/38630537

Research summary

This study investigates the role of Set7 methyltransferase in the phenotypic transition of glomerular endothelial cells under diabetic conditions. The research aims to elucidate how Set7-mediated epigenetic modifications contribute to endothelial dysfunction and the progression of diabetic nephropathy.

Key outcome of the study

Loss of Set7 in endothelial cells prevented the diabetes-induced endothelial-to-mesenchymal transition (EndMT) and preserved glomerular function. These findings suggest that Set7 is a key regulator of endothelial phenotypic changes in diabetic nephropathy.

Mouse model

The study utilized a conditional endothelial-specific Set7 Knockout mouse model developed in collaboration with genOway. This model allows for the deletion of Set7 specifically in endothelial cells, enabling the assessment of its function in vascular biology and diabetic pathology.

TARGET:
Setd7
SET7, KMT7

Keywords

Diabetic nephropathy, Endothelial dysfunction, Epigenetics, EndMT, Kidney disease

Technical specifications

Conditional Knockout, Endothelial-specific deletion, Cre-loxP system, Epigenetic regulation, Disease modeling

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Tissue-specific KO mouse

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