Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 125, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2020.109920
Keywords
Diabetic nephropathy; Epithelial-to-mesenchymal transition; Twist1; miR-2467-3p
Funding
- National Natural Science Foundation of China [81801556, 81500720]
- Joint Funds for the Innovation of Science and Technology, Fujian Province [2017Y9108]
- Natural Science Foundation of Fujian Province [2015J05157]
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Although diabetic nephropathy (DN) is induced by a complicate interplay of multiple factors, the underlying mechanisms remain poorly characterized, even the treatment. Herein, we show that both of DN patients and STZ-induced type 1 diabetic rat exhibit the reduction both of urinary and circulating miR-2467-3p. We identify a negative correlation between miR-2467-3p levels and renal dysfunction. Administration of miR-2467-3p prevents diabetes-induced renal dysfunction and represses renal fibrosis in STZ-induced type 1 diabetic rats. Conversely, anti-miR-2467 overexpression exacerbates renal dysfunction and fibrosis in STZ-induced rats. In diabetic condition, the reduction of miR-2467-3p promotes expression of Twist1, inducing epithelial-to-mesenchymal transition (EMT), resulting in renal fibrosis and kidney dysfunction. Together, our study presents miR-2467/Twist1/EMT as a regulatory axis of renal dysfunction in DN.
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