In sepsis, invading pathogens can induce immune dysregulation in the body, resulting in a pathological syndrome characterized by persistent and excessive inflammation as well as immune suppression [1]. Its high morbidity and mortality rate make it one of the leading causes of death globally, with an estimated 48.9 million people worldwide suffering from sepsis in 2017, of whom about 11 million died [2]. Currently, the treatment of sepsis mainly supports symptomatic treatment, early detection and timely implementation of targeted interventions. Finding effective treatment modalities for sepsis has been a major challenge in acute and critical care.

Cell death can be divided into accidental cell death (ACD) and regulated cell death (RCD). ACD is generally unregulated and is often caused by noxious stimuli that exceed the capacity of the cell to control. RCD is also defined as programmed cell death (PCD) and is usually regulated by signaling pathways [3]. Regulated cell death plays a key role in biological processes such as organismal development, homeostasis, and immunity, helping to clear stress cells, damaged cells, malignant cells, or infected cells. Abnormal RCD can lead to a range of human diseases, including tumors, infectious diseases, metabolic disorders and neurological disorders including sepsis [4]. In recent years, studies of different cell death patterns have revealed that pyroptosis, necroptosis, NETosis, and other cell death patterns are not completely independent. Focusing on the links between different cell death patterns could lead to the search for effective treatments [5]. Death pathways such as pyroptosis, necroptosis and NETosis were found to converge with the gasdermin D(GSDMD), suggesting that the GSDMD is central to pro-inflammatory cell death. Therefore, studying GSDMD can help us identify new therapeutic targets for sepsis.