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.
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.
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.
Diabetic nephropathy, Endothelial dysfunction, Epigenetics, EndMT, Kidney disease
Conditional Knockout, Endothelial-specific deletion, Cre-loxP system, Epigenetic regulation, Disease modeling
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
Certified health status from professional breeders
