Han Weidong, Xie Jiansheng, Li Ling, Liu Zhen, Hu Xun
Cancer Institute, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310009, China.
Apoptosis. 2009 May;14(5):674-86. doi: 10.1007/s10495-009-0334-x.
Degterev et al. previously demonstrated that death receptor mediated apoptosis could be diverted to necroptosis when apoptosis signaling was blocked, suggesting that necroptosis may function as a backup mechanism to insure the elimination of damaged cells under certain conditions when apoptosis was inhibited. Here, we show that shikonin-induced necroptosis can be reverted to apoptosis in the presence of necrostatin-1 (Nec-1), a specific necroptosis inhibitor and that the death mode switch is at least partially due to the conversion from mitochondrial inner membrane permeability to mitochondrial outer membrane permeability, which is associated with Bax translocation. The data combined with the previous reports support a notion that apoptosis and necroptosis may function as reciprocal backup mechanisms of cellular demise. To the best of our knowledge, this is the first study to document a conversion from necroptosis to apoptosis.
德格捷列夫等人先前证明，当凋亡信号被阻断时，死亡受体介导的凋亡可转向坏死性凋亡，这表明坏死性凋亡可能作为一种备用机制，以确保在凋亡受到抑制的某些条件下清除受损细胞。在此，我们表明，在特异性坏死性凋亡抑制剂坏死抑制因子-1（Nec-1）存在的情况下，紫草素诱导的坏死性凋亡可恢复为凋亡，并且死亡模式的转换至少部分归因于从线粒体内膜通透性到线粒体外膜通透性的转变，这与Bax易位有关。这些数据与先前的报道相结合，支持了一个观点，即凋亡和坏死性凋亡可能作为细胞死亡的相互备用机制。据我们所知，这是第一项记录从坏死性凋亡向凋亡转变的研究。
