Open Access<p>LncRNA SNHG16 Aggravates High Glucose-Induced Podocytes Injury in Diabetic Nephropathy Through Targeting miR-106a and Thereby Up-Regulating KLF9</p>
Author(s) -
Xin He,
Xiuya Zeng
Publication year - 2020
Publication title -
diabetes, metabolic syndrome and obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.853
H-Index - 43
ISSN - 1178-7007
DOI - 10.2147/dmso.s271290
Subject(s) - synaptopodin , podocyte , diabetic nephropathy , podocin , viability assay , microrna , apoptosis , cancer research , gene knockdown , chemistry , microbiology and biotechnology , biology , endocrinology , medicine , diabetes mellitus , kidney , biochemistry , gene , proteinuria
Diabetic nephropathy (DN) is one of the major complications of diabetes and podocyte injury plays an important role in the DN pathogenesis. MicroRNA (miR)-106a is predicated to be a target of long noncoding RNA (lncRNA) SNHG16 and has been identified as a therapeutic biomarker for diabetic kidney diseases. However, the role of SNHG16/miR-106a axis in DN has not been illustrated. This study aimed to investigate whether SNHG16 could regulate podocyte injury via miR-106a in DN and uncover the underlying mechanism.