Secondary necrosis in multicellular animals: an outcome of apoptosis with pathogenic implications.
Secondary necrosis in multicellular animals: an outcome of apoptosis with pathogenic implications.
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DOI：
10.1007/s10495-008-0187-8
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发表时间：
2008-04
期刊：
影响因子：
--
通讯作者：
dos Santos NM
中科院分区：
文献类型：
--
作者：
Silva MT;do Vale A;dos Santos NM
在后生动物中，细胞凋亡是发育和组织稳态过程中细胞消除的主要生理过程，并且可以参与病理情况。在体外，细胞凋亡通过执行阶段进行，在此期间启动细胞解体，有或没有碎裂成凋亡小体，但维持接近完整的细胞质膜，随后过渡到坏死细胞消除，传统上称为“继发性坏死”。继发性坏死涉及自水解酶的激活、细胞或凋亡小体的肿胀、细胞质膜的普遍性和不可修复的损伤，并以细胞破裂而告终。在体内，在正常条件下，凋亡细胞或凋亡小体的消除是通过在凋亡的执行阶段期间由吞噬信号的暴露引起的清除剂通过吞噬而去除;如果这种去除失败，则如在体外情况下那样进展为继发性坏死。体内继发性坏死发生在大量细胞凋亡破坏可用的清除能力时，或清除机制直接受损时，并可能导致细胞内容物渗漏，诱导组织损伤和炎症及自身免疫反应。继发性坏死已牵连作为一种致病机制的几种疾病将进行审查。
In metazoans apoptosis is a major physiological process of cell elimination during development and in tissue homeostasis and can be involved in pathological situations. In vitro, apoptosis proceeds through an execution phase during which cell dismantling is initiated, with or without fragmentation into apoptotic bodies, but with maintenance of a near-to-intact cytoplasmic membrane, followed by a transition to a necrotic cell elimination traditionally called “secondary necrosis”. Secondary necrosis involves activation of self-hydrolytic enzymes, and swelling of the cell or of the apoptotic bodies, generalized and irreparable damage to the cytoplasmic membrane, and culminates with cell disruption. In vivo, under normal conditions, the elimination of apoptosing cells or apoptotic bodies is by removal through engulfment by scavengers prompted by the exposure of engulfment signals during the execution phase of apoptosis; if this removal fails progression to secondary necrosis ensues as in the in vitro situation. In vivo secondary necrosis occurs when massive apoptosis overwhelms the available scavenging capacity, or when the scavenger mechanism is directly impaired, and may result in leakage of the cell contents with induction of tissue injury and inflammatory and autoimmune responses. Several disorders where secondary necrosis has been implicated as a pathogenic mechanism will be reviewed.
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