Inflammatory processes that recruit leukocytes to injured or infected tissues are crucial for tissue repair and the elimination of pathogens. However, excessive or chronic inflammation promotes tissue damage and disease, as in arthritis, atherosclerosis, inflammatory bowel disease, and COVID-19. Intracellular constituents released from dying cells are among the stimuli that trigger proinflammatory gene expression programs in innate immune cells. We explore how programmed cell death mechanisms—apoptosis, necroptosis, and pyroptosis—may contribute to inflammatory disease. We discuss inhibition of cell death as a potential therapeutic strategy, focusing on the targets RIPK1 (receptor interacting serine/threonine kinase 1), NLRP3 (NLR family pyrin domain containing 3), and GSDMD (gasdermin D) as important mediators of lytic cell death. We also consider the potential benefits of limiting membrane rupture rather than cell death by targeting NINJ1.

中文翻译：

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垂死的细胞助长了炎症的火焰

将白细胞募集到受伤或感染组织的炎症过程对于组织修复和消除病原体至关重要。然而，过度或慢性炎症会促进组织损伤和疾病，如关节炎、动脉粥样硬化、炎症性肠病和 COVID-19。垂死细胞释放的细胞内成分是触发先天免疫细胞中促炎基因表达程序的刺激因素之一。我们探索程序性细胞死亡机制——细胞凋亡、坏死性凋亡和细胞焦亡——可能如何导致炎症性疾病。我们讨论抑制细胞死亡作为一种潜在的治疗策略，重点关注靶点 RIPK1（受体相互作用丝氨酸/苏氨酸激酶 1）、NLRP3（含有 3 的 NLR 家族 pyrin 结构域）和 GSDMD（gasdermin D）作为裂解细胞死亡的重要介质.