细胞焦亡在急性胰腺炎中的作用及临床转化:研究进展
The Role of Pyroptosis in Acute Pancreatitis and Its Clinical Translation: Research Progress
DOI: 10.12677/acm.2026.1682793, PDF,   
作者: 陈卫强*:承德医学院研究生学院,河北 承德;孙建利#:承德市中心医院急诊科,河北 承德
关键词: 急性胰腺炎;重症急性胰腺炎;细胞焦亡;NLRP3炎症小体;GSDMD;亚致死性焦亡;GSDME;Acute Pancreatitis; Severe Acute Pancreatitis; Pyroptosis; NLRP3 Inflammasome; GSDMD; Sublytic Pyroptosis; GSDME
摘要: 急性胰腺炎是急诊常见急腹症,重症患者可发生持续器官功能衰竭。细胞焦亡以炎症小体激活、炎症性caspase切割gasdermin并形成膜孔为核心,可促进IL-1β、IL-18释放和炎症放大。研究提示,NLRP3/Caspase-1/GSDMD及Caspase-4/5/11/GSDMD通路参与腺泡细胞损伤、免疫细胞激活、肠屏障破坏和远隔器官损害。本文综述其机制、病理作用及转化挑战。在此基础上,本文进一步补充讨论亚致死性焦亡、GSDME等GSDM家族成员,以及焦亡标志物在AP早期预警、病情分层和临床试验设计中的潜在价值。
Abstract: Acute pancreatitis is a common acute abdominal disease in emergency and digestive medicine. Although most cases are mild and self-limited, some patients progress to moderately severe or severe acute pancreatitis with persistent organ failure. Pyroptosis is an inflammatory form of programmed cell death characterized by inflammasome activation, inflammatory caspase-mediated gasdermin cleavage, membrane pore formation, and the release of interleukin-1β and interleukin-18. Increasing evidence suggests that the NLRP3/Caspase-1/GSDMD axis and the non-canonical Caspase-4/5/11/GSDMD pathway may participate in acinar cell injury, immune amplification, intestinal barrier disruption, and distant organ damage in acute pancreatitis. This review summarizes the molecular basis, pathological roles, potential interventions, and translational challenges of pyroptosis in acute pancreatitis. In addition, this review discusses sublytic pyroptosis, GSDME and other gasdermin family members, and the potential value of pyroptosis-related biomarkers in early warning, severity stratification, and clinical trial design for acute pancreatitis.
文章引用:陈卫强, 孙建利. 细胞焦亡在急性胰腺炎中的作用及临床转化:研究进展[J]. 临床医学进展, 2026, 16(8): 263-269. https://doi.org/10.12677/acm.2026.1682793

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