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In the past few decades, there has been a large amount of evidence to highlight the pivotal role of oxidative stress in the development and progression of DKD. However, the detailed molecular mechanisms are not fully elucidated. A new sight has been established that the mitochondrial acetyltransferase GCN5L1 participates in cellular redox homeostasis maintenance in DKD. Firstly, we found that the expression of GCN5L1 is significantly elevated both in human and mouse kidney tissues with DKD and in hyperglycemic renal tubular epithelial cells (TECs), while deletion of GCN5L1 could effectively ameliorate oxidative stress\u2010induced renal injury in DKD. Furthermore, deletion of GCN5L1 could reduce MnSOD acetylation on lysine 68 and activate its activity, thereby scavenging excessive ROS and relieving oxidative stress\u2010induced renal inflammation and fibrosis. In general, GCN5L1\u2010mediated acetylation of MnSOD exacerbated oxidative stress\u2010induced renal injury, suggesting that GCN5L1 might be a potential intervention target in DKD.<\/jats:p>","DOI":"10.1155\/2021\/6691226","type":"journal-article","created":{"date-parts":[[2021,2,18]],"date-time":"2021-02-18T19:13:49Z","timestamp":1613675629000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["General Control of Amino Acid Synthesis 5\u2010Like 1\u2010Mediated Acetylation of Manganese Superoxide Dismutase Regulates Oxidative Stress in Diabetic Kidney 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