Year: 2025
Type: article
Abstract: 细胞焦亡是由gasdermin家族蛋白介导的炎性细胞死亡方式，涉及细胞膜上孔的形成和炎性细胞因子的释放。细胞焦亡在宿主抵抗微生物感染中起着至关重要的作用，与自身免疫性疾病的发生发展密切相关。炎症性肠病包括溃疡性结肠炎和克罗恩病，是一类以肠道慢性炎症为特征的疾病，其发病机制涉及遗传、免疫、微生物及环境等。在炎症性肠病患者中，过度激活的细胞焦亡，导致炎症反应加剧、肠道屏障功能受损、肠道菌群失调以及免疫细胞异常活化等，从而推动疾病进程。本文旨在阐述细胞焦亡的分子机制及其在炎症性肠病中作用的研究进展，为炎症性肠病提供新的治疗思路。Pyroptosis is an inflammatory form of programmed cell death mediated by the gasdermin family of proteins, involving the formation of pores in the cell membrane and the release of inflammatory cytokines. Pyroptosis plays a crucial role in the host’s defense against microbial infections and is closely associated with the development of autoimmune diseases. Inflammatory bowel disease (IBD), which includes ulcerative colitis and Crohn’s disease, is characterized by chronic intestinal inflammation. Its pathogenesis involves genetic, immune, microbial, and environmental factors. In patients with IBD, overactivated pyroptosis exacerbates the inflammatory response, impairs the intestinal barrier function, disrupts the gut microbiota, and leads to abnormal activation of immune cells, thereby promoting disease progression. This review aims to elaborate on the mechanisms of pyroptosis and the latest research progress on its role in IBD, providing novel therapeutic strategies for this disease.
Source: Pharmacy Information
Author: 磊 高
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: hybrid
OpenAlex ID: W4412513571