PGC-1α alleviates mitochondrial dysfunction via TFEB-mediated autophagy in cisplatin-induced acute kidney injury
Longhui Yuan, Yujia Yuan, Fei Liu, Lan Li, Jingping Liu, Younan Chen, Jingqiu Cheng, Yanrong Lu
Abstract
overexpression of PGC-1α or ZLN005 treatment inhibited cell apoptosis and mitochondrial dysfunction induced by cisplatin. Moreover, ZLN005 treatment increased the expression of LC3-II and co-localization between LC3 and mitochondria, suggesting that the mitophagy was activated. Furthermore, PGC-1α-mediated the activation of mitophagy was reliant on the increased expression of TFEB, and the protective effects were abrogated in TFEB-knockdown cells. These data suggest that the activation of PGC-1α could alleviate mitochondrial dysfunction and kidney injury in AKI mice via TFEB-mediated autophagy.
Topics & Concepts
AutophagyTFEBCisplatinAcute kidney injuryMedicineMitochondrionCancer researchKidneyPharmacologyApoptosisChemistryBiologyInternal medicineCell biologyChemotherapyBiochemistryChemotherapy-induced organ toxicity mitigationAcute Kidney Injury ResearchDialysis and Renal Disease Management