MicroRNA-709 Mediates Acute Tubular Injury through Effects on Mitochondrial Function

• DOI: 10.1681/asn.2017040381
• Publication Date: 2017-10-18T00:25:24Z
• Authors: Yan Guo; Jiajia Ni; Shuang Chen; Mi Bai; Jiajuan Lin; Guixia Ding; Yue Zhang; Pingping Sun; Zhanjun Jia; Songming Huang; Li Yang; Aihua Zhang
• Keywords: TFAM

Mitochondrial dysfunction has important roles in the pathogenesis of AKI, yet therapeutic approaches to improve mitochondrial function remain limited. In this study, we investigated pathogenic role microRNA-709 (miR-709) mediating impairment and tubular cell death AKI. a cisplatin-induced AKI mouse model biopsy samples human kidney tissue, miR-709 was significantly upregulated proximal cells (PTCs). The expression renal PTCs patients with correlated severity injury. cultured PTCs, overexpression markedly induced apoptosis, inhibition ameliorated Further analyses showed that transcriptional factor A (TFAM) is target gene miR-709, genetic restoration TFAM attenuated injury by cisplatin or vitro Moreover, antagonizing an antagomir dramatically mice. Collectively, our results suggest via negative regulation subsequent dysfunction. These findings reveal acute novel for treatment