Abstract：
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.
摘要：
急性肾损伤(AKI)是脓毒症的常见和严重并发症,其特征在于显著的死亡率和发病率。然而,脓毒症急性肾损伤(S-AKI)的发病机制尚不清楚。代谢重编程，最初被称为癌症中的Warburg效应，与S-AKI密切相关。在脓毒症发作时,炎症细胞和肾实质细胞，比如巨噬细胞，中性粒细胞和肾小管上皮细胞，经历向有氧糖酵解的代谢转变，以增强促炎反应并增强细胞对败血症刺激的抵抗力。随着疾病的进展,这些细胞恢复到氧化磷酸化，从而促进抗炎反应和增强功能恢复。线粒体动力学和代谢重编程的改变对于S-AKI期间发生的能量变化至关重要。在这次审查中,我们总结了目前对S-AKI代谢重编程发病机制的认识，重点关注所涉及的每种细胞类型。通过确定相关关键监管因素，我们还探索了潜在的代谢重编程相关治疗靶点,用于治疗S-AKI.
