急性肾损伤（AKI）是脓毒症常见且严重的并发症，其特点是死亡率和发病率很高。然而，脓毒性急性肾损伤（S-AKI）的发病机制仍然难以捉摸。代谢重编程最初被称为癌症中的 Warburg 效应，与 S-AKI 密切相关。脓毒症发作时，炎症细胞和肾实质细胞，如巨噬细胞、中性粒细胞和肾小管上皮细胞，都会经历向有氧糖酵解的代谢转变，以放大促炎反应并增强细胞对脓毒症刺激的抵抗力。随着疾病的进展，这些细胞恢复氧化磷酸化，从而促进抗炎反应并增强功能恢复。线粒体动力学和代谢重编程的改变是 S-AKI 期间发生的能量变化的核心。在这篇综述中，我们总结了目前对 S-AKI 代谢重编程发病机制的理解，重点关注涉及的每种细胞类型。通过确定相关的关键调控因素，我们还探索了用于 S-AKI 管理的潜在代谢重编程相关治疗靶点。版权所有 © 2024。由 Elsevier Inc. 出版。

Acute kidney injury (AKI) is a frequent and severe complication of sepsis and is characterized by significant mortality and morbidity. However, the pathogenesis of septic acute kidney injury (S-AKI) remains elusive. Metabolic reprogramming, which was originally referred to as the Warburg effect in cancer, is strongly related to S-AKI. At the onset of sepsis, both inflammatory cells and renal parenchymal cells, such as macrophages, neutrophils and renal tubular epithelial cells, undergo metabolic shifts toward aerobic glycolysis to amplify proinflammatory responses and fortify cellular resilience to septic stimuli. As the disease progresses, these cells revert to oxidative phosphorylation, thus promoting anti-inflammatory reactions and enhancing functional restoration. Alterations in mitochondrial dynamics and metabolic reprogramming are central to the energetic changes that occur during S-AKI. In this review, we summarize the current understanding of the pathogenesis of metabolic reprogramming in S-AKI, with a focus on each cell type involved. By identifying relevant key regulatory factors, we also explored potential metabolic reprogramming-related therapeutic targets for the management of S-AKI.Copyright © 2024. Published by Elsevier Inc.