Zong Wei-Xing, Thompson Craig B
Department of Molecular Genetics and Microbiology, State University of New York at Stony Brook, New York 11794, USA.
Genes Dev. 2006 Jan 1;20(1):1-15. doi: 10.1101/gad.1376506.
Organismal homeostasis depends on an intricate balance between cell death and renewal. Early pathologists recognized that this balance could be disrupted by the extensive damage observed in internal organs during the course of certain diseases. This form of tissue damage was termed "necrosis", derived from the Greek "nekros" for corpse. As it became clear that the essential building block of tissue was the cell, necrosis came to be used to describe pathologic cell death. Until recently, necrotic cell death was believed to result from injuries that caused an irreversible bioenergetic compromise. The cell dying by necrosis has been viewed as a victim of extrinsic events beyond its control. However, recent evidence suggests that a cell can initiate its own demise by necrosis in a manner that initiates both inflammatory and/or reparative responses in the host. By initiating these adaptive responses, programmed cell necrosis may serve to maintain tissue and organismal integrity.
机体的稳态依赖于细胞死亡与更新之间的复杂平衡。早期病理学家认识到,在某些疾病过程中,内部器官所观察到的广泛损伤可能会破坏这种平衡。这种形式的组织损伤被称为“坏死”,源自希腊语“nekros”,意为尸体。随着组织的基本构建单元是细胞这一点变得清晰,坏死开始被用于描述病理性细胞死亡。直到最近,坏死性细胞死亡被认为是由导致不可逆生物能量受损的损伤所引起的。因坏死而死亡的细胞被视为超出其控制范围的外在事件的受害者。然而,最近的证据表明,细胞可以通过坏死启动自身的死亡,这种方式会在宿主体内引发炎症和/或修复反应。通过启动这些适应性反应,程序性细胞坏死可能有助于维持组织和机体的完整性。