目的：GasderminD（GSDMD）是由Gasdermin家族GSDMD基因编码的细胞质蛋白，是焦亡的最终执行者。焦亡是一种调节细胞死亡的裂解和炎症模式，最终导致细胞肿胀和破裂。在脓毒症中，宿主对感染的反应失调经常导致炎症反应和免疫抑制，最终导致多器官功能障碍。焦亡调节先天免疫防御，在炎性细胞死亡过程中发挥重要作用，从GSDMD到焦亡的整个途径中没有任何联系会导致细菌清除受到阻碍。在正常情况下,焦亡的过程比细胞凋亡快得多，对身体的威胁也更大。
方法：我们使用关键词败血症对相关综述和实验文章进行了系统综述，GasderminD,和PubMed中的焦亡，Scopus,谷歌学者，和WebofScience数据库。
结论：结合脓毒症的发病机制，不难发现，焦亡在细菌炎症和败血症中起着关键作用。因此,GSDMD抑制剂可作为靶向药物,通过减少脓毒症的发生来治疗脓毒症。本文就GSDMD在脓毒症中的关键作用作一综述。
OBJECTIVE: Gasdermin D (GSDMD) is a cytoplasmic protein that is encoded by the gasdermin family GSDMD gene and is the ultimate executor of pyroptosis. Pyroptosis is a mode of lysis and inflammation that regulates cell death, ultimately leading to cell swelling and rupture. In sepsis, a dysregulated host response to infection frequently results in hyperinflammatory responses and immunosuppression, eventually leading to multiple organ dysfunction. Pyroptosis regulates innate immune defenses and plays an important role in the process of inflammatory cell death, and the absence of any link in the entire pathway from GSDMD to pyroptosis causes bacterial clearance to be hampered. Under normal conditions, the process of pyroptosis occurs much faster than apoptosis, and the threat to the body is also much greater.
METHODS: We conducted a systematic
review of relevant reviews and experimental articles using the keywords sepsis, Gasdermin D, and Pyroptosis in the PubMed, Scopus, Google Scholar, and Web of Science databases.
CONCLUSIONS: Combined with the pathogenesis of sepsis, it is not difficult to find that pyroptosis plays a key role in bacterial inflammation and sepsis. Therefore, GSDMD inhibitors may be used as targeted drugs to treat sepsis by reducing the occurrence of pyroptosis. This
review mainly discusses the key role of GSDMD in sepsis.
