Cell death and fibrogenesis.
Cell death and fibrogenesis.
复制标题
细胞死亡和纤维发生。
DOI：
10.1055/s-0030-1255352
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发表时间：
2010-08
影响因子：
4.2
通讯作者：
Imaeda A
中科院分区：
文献类型：
--
作者：
Mehal W;Imaeda A
纤维化是慢性肝损伤的常见特征，由肝脏内的细胞死亡引起。肝细胞死亡导致凋亡小体和其他细胞碎片被肝星状细胞(HSCs)吞噬，导致其激活、增殖、分化和基质沉积。细胞死亡的这种促纤维化作用与HSC死亡的抗纤维化作用相平衡。许多HSC存活信号来自细胞外基质，主动促凋亡信号由免疫细胞，特别是自然杀伤(NK)细胞提供。静止的HSC对凋亡信号具有相对的抵抗力，但在激活后变得敏感。NK细胞在诱导HSC凋亡中的重要作用可能解释了与免疫抑制(例如，在移植受者中)和HIV感染相关的纤维化增加的原因。肝星状细胞也会经历衰老，这限制了它们的功能，并使它们对凋亡敏感。
Fibrosis is a common feature of chronic liver injury and is initiated by cell death inside the liver. Hepatocyte death results in apoptotic bodies and other cellular debris, which are phagocytosed by hepatic stellate cells (HSCs), resulting in their activation, proliferation, differentiation, and matrix deposition. This profibrotic effect of cellular death is balanced by an antifibrotic effect of HSC death. Many HSC survival signals are obtained from the extracellular matrix, and active proapoptotic signals are provided by immune cells, particularly natural killer (NK) cells. Quiescent HSCs are relatively resistant to apoptotic signals but become sensitive after activation. The important role of NK cells in inducing HSC apoptosis may explain the increased fibrosis associated with immune suppression (e.g., in the transplant recipient) and HIV infection. HSCs also undergo senescence, which limits their function and sensitizes them to apoptosis.
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影响因子：
29.4
作者：
Issa, R;Zhou, XY;Iredale, JP
通讯作者：
Iredale, JP
影响因子：
7.3
作者：
Chan, Edwin S. L.;Montesinos, Maria Carmen;Cronstein, Bruce N.
通讯作者：
Cronstein, Bruce N.
影响因子：
13.5
作者：
Gong, WR;Pecci, A;Gressner, AM
通讯作者：
Gressner, AM
DOI：
10.1124/jpet.103.060129
发表时间：
2004-03-01
影响因子：
3.5
作者：
Canbay, A;Feldstein, A;Gores, GJ
通讯作者：
Gores, GJ
影响因子：
--
作者：
Cariers, A;Reinehr, R;Häussinger, D
通讯作者：
Häussinger, D