biostudies-literatureXin WNatural Science Foundation of Chongqing Science & Technology CommissionNational Key R&D Program of ChinaNatural Science Foundation of ChinaChongqing Science and Technology Talent ProgramKey program of the Natural Science Foundation of Chinae2412233https://www.ebi.ac.uk/biostudies/studies/S-EPMC11809329biostudies-literatureUnknown12(6)Acute kidney injury (AKI) is a prevalent clinical syndrome with high morbidity and mortality. Accumulating studies suggest mitochondrial dysfunction as the typical characteristics and key process of AKI, but the underlying mechanism remains elusive. The YME1-like 1 (YME1L1) ATPase, an inner mitochondrial membrane protein, is screened and identified to be downregulated in renal tubular epithelial cells of various mouse models and patients of AKI. Dramatically, restoration of YME1L1 expression significantly alleviates cisplatin-induced AKI and subsequent chronic kidney disease (CKD) through attenuating mitochondrial dysfunction via maintaining optic atrophy 1 (OPA1)-mediated mitochondrial energy metabolism homeostasis. Mechanistically, the upregulated expression of sterol regulatory element Advanced science (Weinheim, Baden-Wurttemberg, Germany)SREBP1c-Mediated Transcriptional Repression of YME1L1 Contributes to Acute Kidney Injury by Inducing Mitochondrial Dysfunction in Tubular Epithelial Cells.PMC118093292022YFC2502500/2022YFC250250182322012CQYC20220511193cstb2022nscq-msx0220U22A20279cstc2021ycjh-bgzxm014582030023Peng YXiong JGong SLiao WYao MQin SLi YHuang YLan QHuang XWang YXin WZhao JMao YZhou JfalseSREBP1c-Mediated Transcriptional Repression of YME1L1 Contributes to Acute Kidney Injury by Inducing Mitochondrial Dysfunction in Tubular Epithelial Cells.Acute kidney injury (AKI) is a prevalent clinical syndrome with high morbidity and mortality. Accumulating studies suggest mitochondrial dysfunction as the typical characteristics and key process of AKI, but the underlying mechanism remains elusive. The YME1-like 1 (YME1L1) ATPase, an inner mitochondrial membrane protein, is screened and identified to be downregulated in renal tubular epithelial cells of various mouse models and patients of AKI. Dramatically, restoration of YME1L1 expression significantly alleviates cisplatin-induced AKI and subsequent chronic kidney disease (CKD) through attenuating mitochondrial dysfunction via maintaining optic atrophy 1 (OPA1)-mediated mitochondrial energy metabolism homeostasis. Mechanistically, the upregulated expression of sterol regulatory element 2025-01-01T00:00:00Z2025 Feb2025-04-04T02:38:43.693Z2025-04-04T02:38:43.693ZS-EPMC118093293968075210.1002/advs.202412233