ets1 associates with KMT5A to participate in high glucose-mediated EndMT via upregulation of PFN2 expression in diabetic nephropathy

• Published in: Molecular medicine (Cambridge, Mass.) Vol. 27; no. 1; pp. 74 - 19
• Main Authors: Lu, Lihong, Zhong, Ziwen, Gu, Jiahui, Nan, Ke, Zhu, Minmin, Miao, Changhong
• Format: Journal Article
• Language: English
• Published: England BioMed Central 08.07.2021; BMC
• Subjects: Aged; Animals; Binding Sites; Biomarkers; Diabetic Nephropathies - etiology; Diabetic Nephropathies - metabolism; Diabetic Nephropathies - pathology; Diabetic nephropathy; Disease Models, Animal; Disease Susceptibility; EndMT; Epithelial-Mesenchymal Transition - genetics; ets1; Female; Gene Expression; Gene Expression Profiling; Glucose - metabolism; Histone-Lysine N-Methyltransferase - genetics; Histone-Lysine N-Methyltransferase - metabolism; Human Umbilical Vein Endothelial Cells; Humans; Immunohistochemistry; KMT5A; Male; Middle Aged; Models, Biological; PFN2; Profilins - genetics; Profilins - metabolism; Protein Binding; Proto-Oncogene Protein c-ets-1 - genetics; Proto-Oncogene Protein c-ets-1 - metabolism; Rats; Diabetic nephropathy; ets1; KMT5A; EndMT; PFN2

Diabetic nephropathy (DN) is currently the leading cause of end-stage renal disease globally. The endothelial-to-mesenchymal transition (EndMT) of glomerular endothelial cells has been reported to play a crucial role in DN. As a specific form of epithelial-to-mesenchymal transition, EndMT and epithe...