Sepsis is a severe and life-threatening disease caused by infection, characterized by a dysregulated immune response. Unfortunately, effective treatment strategies for sepsis are still lacking. The intricate interplay between metabolism and the immune system limits the treatment options for sepsis. During sepsis, there is a profound shift in cellular energy metabolism, which triggers a metabolic reprogramming of immune cells. This metabolic alteration impairs immune responses, giving rise to excessive inflammation and immune suppression. Recent research has demonstrated that UCP2 not only serves as a critical target in sepsis but also functions as a key metabolic switch involved in immune cell-mediated inflammatory responses. However, the regulatory mechanisms underlying this modulation are complex. This article focuses on UCP2 as a target and discusses metabolic reprogramming during sepsis and the complex regulatory mechanisms between different stages of inflammation. Our research indicates that overexpression of UCP2 reduces the Warburg effect, restores mitochondrial function, and improves the prognosis of sepsis. This discovery aims to provide a promising approach to address the significant challenges associated with metabolic dysfunction and immune paralysis.

脓毒症是一种由感染引起的严重且危及生命的疾病，其特征是免疫反应失调。不幸的是，仍然缺乏针对脓毒症的有效治疗策略。新陈代谢和免疫系统之间复杂的相互作用限制了脓毒症的治疗选择。在脓毒症期间，细胞能量代谢发生深刻变化，从而引发免疫细胞的代谢重编程。这种代谢改变会损害免疫反应，导致过度炎症和免疫抑制。最近的研究表明，UCP2 不仅是脓毒症的关键靶点，而且还是参与免疫细胞介导的炎症反应的关键代谢开关。然而，这种调节背后的调节机制很复杂。本文重点以 UCP2 作为靶点，讨论脓毒症期间的代谢重编程以及炎症不同阶段之间的复杂调节机制。我们的研究表明，UCP2 的过度表达可降低 Warburg 效应，恢复线粒体功能，并改善脓毒症的预后。这一发现旨在提供一种有前途的方法来解决与代谢功能障碍和免疫麻痹相关的重大挑战。