Mitochondrial ROS promote mitochondrial dysfunction and inflammation in ischemic acute kidney injury by disrupting TFAM-mediated mtDNA maintenance
Meng Zhao, Yizhuo Wang, Ling Li, Shuyun Liu, Chengshi Wang, Yujia Yuan, Guang Yang, Younan Chen, Jingqiu Cheng, Yanrong Lu, Jingping Liu
Abstract
mtROS can promote renal injury by suppressing TFAM-mediated mtDNA maintenance, resulting in decreased mitochondrial energy metabolism and increased cytokine release. TFAM defects may be a promising target for renal repair after IRI-AKI.
Topics & Concepts
TFAMMitochondrial DNAInflammationMitochondrionAcute kidney injuryMedicineBiologyCell biologyMitochondrial biogenesisImmunologyInternal medicineGeneticsGeneAcute Kidney Injury ResearchOrgan Transplantation Techniques and OutcomesChronic Kidney Disease and Diabetes