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贮脂细胞经过激活、刺激性增殖、表型转换后分泌大量的细胞外基质和基质金属硫蛋白酶抑制剂 (TIMPs)而在肝纤维化中发挥了关键作用。但随着贮脂细胞的激活 ,其凋亡敏感性发生改变 ,通过Fas依赖途径发生凋亡 ,其数量明显减少 ,细胞外基质合成和TIMPs的表达快速下降 ,而使肝纤维化发生逆转。这一过程涉及贮脂细胞中凋亡和抑凋亡基因的表达变化。提示通过诱导激活的贮脂细胞凋亡 ,可能为肝纤维化的逆转治疗提供一新的乐观手段。
The fat-storage cells play a key role in hepatic fibrosis after activation, stimulatory proliferation, phenotypic diversification of large extracellular matrix and matrix metallothionein inhibitors (TIMPs). However, with the activation of the fat-storing cells, the apoptosis sensitivity changes, and the apoptosis occurs through the Fas-dependent pathway. The number of apoptotic cells is obviously decreased, the synthesis of extracellular matrix and the expression of TIMPs are rapidly decreased, and the liver fibrosis is reversed. This process involves changes in the expression of apoptotic and anti-apoptotic genes in fat-storing cells. It is suggested that apoptosis induced by activated fat-storage cells may provide a new optimism for the reversal of liver fibrosis.