Department of Infectious Diseases, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, China.
Department of Intensive Care Unit, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, China.
Int Immunopharmacol. 2024 Nov 15;141:113006. doi: 10.1016/j.intimp.2024.113006. Epub 2024 Aug 29.
Pyroptosis, a newly identified form of programmed cell death intertwined with inflammatory responses, is facilitated by the Gasdermin family's pore-forming activity, leading to cell lysis and the release of pro-inflammatory cytokines. This process is a double-edged sword in innate immunity, offering protection against pathogens while risking excessive inflammation and tissue damage when dysregulated. Specifically, pyroptosis operates through two distinct signaling pathways, namely the Caspase-1 pathway and the Caspase-4/5/11 pathway. In the context of chronic liver diseases like fibrosis and cirrhosis, inflammation emerges as a central contributing factor to their pathogenesis. The identification of inflammation is characterized by the activation of innate immune cells and the secretion of pro-inflammatory cytokines such as IL-1α, IL-1β, and TNF-α. This review explores the interrelationship between pyroptosis and the inflammasome, a protein complex located in liver cells that recognizes danger signals and initiates Caspase-1 activation, resulting in the secretion of IL-1β and IL-18. The article delves into the influence of the inflammasome and pyroptosis on various liver disorders, with a specific focus on their molecular and pathophysiological mechanisms. Additionally, the potential therapeutic implications of targeting pyroptosis for liver diseases are highlighted for future consideration.
细胞焦亡是一种新发现的与炎症反应交织在一起的程序性细胞死亡形式,它是由 GSDMD 家族的成孔活性所介导的,导致细胞裂解和促炎细胞因子的释放。在先天免疫中,这一过程是一把双刃剑,既能抵御病原体,又存在失调时引发过度炎症和组织损伤的风险。具体来说,细胞焦亡通过两种不同的信号通路发挥作用,即 Caspase-1 通路和 Caspase-4/5/11 通路。在纤维化和肝硬化等慢性肝脏疾病中,炎症是其发病机制的一个核心因素。炎症的识别特征是先天免疫细胞的激活和促炎细胞因子如 IL-1α、IL-1β 和 TNF-α 的分泌。本综述探讨了细胞焦亡与炎症小体之间的相互关系,炎症小体是一种位于肝细胞中的蛋白复合物,能够识别危险信号并启动 Caspase-1 的激活,导致 IL-1β 和 IL-18 的分泌。文章深入探讨了炎症小体和细胞焦亡对各种肝脏疾病的影响,并特别关注了它们的分子和病理生理学机制。此外,还强调了针对细胞焦亡治疗肝脏疾病的潜在治疗意义,以供未来考虑。