Sepsis is defined as a life-threatening disease involving multiple organ dysfunction caused by dysregulated host responses to infection. To date, sepsis remains a dominant cause of death among critically ill patients. Pyroptosis is a unique form of programmed cell death mediated by the gasdermin family of proteins and causes lytic cell death and release of proinflammatory cytokines. Although there might be some positive aspects to pyroptosis, it is regarded as harmful during sepsis and needs to be restricted. Autophagy was originally characterized as a homeostasis-maintaining mechanism in living cells. In the past decade, its function in negatively modulating pyroptosis and inflammation during sepsis has attracted increased attention. Here, we present a comprehensive review of the regulatory effect of autophagy on pyroptosis during sepsis, including the latest advances in our understanding of the mechanism and signaling pathways involved, as well as the potential therapeutic application in sepsis.

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细胞焦亡的自噬调节：脓毒症的机制和医学意义

脓毒症被定义为一种危及生命的疾病，涉及由宿主对感染的反应失调引起的多器官功能障碍。迄今为止，脓毒症仍然是危重患者死亡的主要原因。Pyroptosis 是一种独特的程序性细胞死亡形式，由 gasdermin 蛋白家族介导，并导致裂解细胞死亡和促炎细胞因子的释放。尽管焦亡可能有一些积极的方面，但它在败血症期间被认为是有害的，需要加以限制。自噬最初被描述为活细胞中的一种稳态维持机制。在过去的十年中，其在脓毒症期间负性调节细胞焦亡和炎症的功能引起了越来越多的关注。在这里，我们全面回顾了自噬对脓毒症期间细胞焦亡的调节作用，