乳酸代谢重编程在脓毒症免疫调控中的研究进展

Research progress on lactate metabolism reprogramming in regulation of immune function in sepsis

  • 摘要: 脓毒症是一种由宿主对感染的免疫-炎症反应失调所致的危及生命的多器官功能障碍综合征。血清乳酸水平升高被视为组织低灌注与无氧代谢的生物标志物,脓毒症患者常表现为高乳酸血症,临床上用于评估疾病严重程度及预后。近年研究表明,乳酸不仅是代谢终产物,更是作为一种关键的免疫代谢调节分子,在脓毒症病理进程中发挥多重作用。本文旨在整合基础与临床证据,阐明乳酸从传统灌注标志物向功能性免疫代谢介质的角色转变,为脓毒症的精准评估与干预提供新视角。

     

    Abstract: Sepsis is a life-threatening multiple organ dysfunction syndrome caused by the dysregulation of the host's immune-inflammatory response to infection. Elevated serum lactate levels are regarded as biomarkers of tissue hypoperfusion and anaerobic metabolism. Sepsis patients often present with hyperlactatemia, which is clinically used to assess disease severity and prognosis. Recent studies have shown that lactate is not only an end-product of metabolism but also serves as a crucial immunometabolic regulatory molecule, playing multiple roles in the pathological process of sepsis. This article aimed to integrate basic and clinical evidence to elucidate the role transformation of lactate from a traditional perfusion marker to a functional immunometabolic mediator, providing a new perspective for the precise assessment and intervention of sepsis.

     

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