miR-1187 induces podocyte injury and diabetic nephropathy through autophagy.

Abstract

MicroRNAs plays important roles in the progression of diabetic nephropathy (DN) and podocyte injury. This study aimed to investigate the role and regulation mechanism of miR-1187 during the development of DN and podocyte injury. The content of miR-1187 in podocytes was up-regulated under high glucose (HG) treatment and increased in kidney tissue of db/db mice (DN model mice) compared with control db/m mice. The administration of miR-1187 inhibitor could decrease podocyte apoptosis induced by HG and attenuate the decline in renal function and reduce proteinuria as well as glomerular apoptosis in db/db mice. Mechanistically, miR-1187 could inhibit the autophagy level in HG-exposed podocytes and glomerulus of DN mice. Moreover, miR-1187 inhibitor could reduce HG-stimulated podocyte injury and autophagy flux inhibition. The mechanism may depend on autophagy. In conclusion, targeting miR-1187 may be a new therapeutic target for improving the high glucose damage of podocytes and the progression of DN.