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首页> 美国卫生研究院文献>Cell Death and Differentiation >Programmed Necrosis and Disease:We interrupt your regular programming to bring you necroinflammation
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Programmed Necrosis and Disease:We interrupt your regular programming to bring you necroinflammation

机译：程序性坏死和疾病：我们打断您的常规程序以给您带来坏死性炎症

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摘要

Molecular pathways of cell death and their roles in inflammation. Depending on death stimuli and context, live cells can undergo apoptosis or programmed necrosis. When caspase 3/7-dependent apoptotic cells are timely scavenged by efferocytosis, efferocytes like macrophages release anti-inflammatory cytokines and prevent unwanted inflammation. In the absence of effective clearance, apoptotic cells are proceeded to secondary necrosis and elicit some inflammatory responses. Upon damage signals such as infection or metabolic stress, cells trigger genetically programmed necrosis. Necroptosis and pyroptosis are RIPK3-MLKL- and inflammasome-GSDMD-mediated processes, respectively, displaying typical lytic morphology similar to primary necrosis. In contrast, ferroptosis is triggered by lipid peroxidation, and shows damaged mitochondria and reduced cellular volume. NETosis is a ROS-induced lytic cell death resulting in the extrusion of neutrophil extracellular traps (NETs), consisting of genomic DNA complexed with cellular proteins. Programmed necrotic cells generally release DAMPs and inflammatory cytokines that stimulate innate immune cells and promote necroinflammation
机译：细胞死亡的分子途径及其在炎症中的作用。根据死亡刺激和环境，活细胞可能会发生凋亡或程序性坏死。当通过胞吞作用及时清除caspase 3/7依赖性凋亡细胞时，像巨噬细胞这样的泡腾细胞会释放抗炎细胞因子，并防止有害的炎症。在没有有效清除的情况下，凋亡细胞会进行继发性坏死并引发一些炎症反应。受到感染或代谢应激等损伤信号后，细胞会触发基因程序性坏死。坏死和发烧分别是RIPK3-MLKL-和炎性小体-GSDMD介导的过程，显示出与原发性坏死相似的典型裂解形态。相反，肥大症是由脂质过氧化作用触发的，显示线粒体受损，细胞体积减少。 NETosis是由ROS诱导的裂解细胞死亡，导致嗜中性粒细胞外捕获物（NETs）挤出，后者由与细胞蛋白复合的基因组DNA组成。程序性坏死细胞通常会释放DAMPs和炎性细胞因子，从而刺激先天免疫细胞并促进坏死性炎症

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