Autophagy as a protective response to Bnip3-mediated apoptotic signaling in the heart
Autophagy as a protective response to Bnip3-mediated apoptotic signaling in the heart
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DOI：
10.4161/auto.2947
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发表时间：
2006-10-01
期刊：
影响因子：
13.3
通讯作者：
Gustafsson, Asa B.
中科院分区：
文献类型：
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作者：
Hamacher-Brady, Anne;Brady, Nathan R.;Gustafsson, Asa B.
Bnip 3是“仅BH 3 "Bd-2亚家族的成员，其涉及凋亡、（1）坏死（2）和自噬性细胞死亡。（3，4）我们最近报道了Bnip 3是离体心脏缺血/再灌注（I/R）后线粒体功能障碍和细胞死亡的关键介质。(5)此外，我们发现Bnip 3参与I/R中自噬的上调，并且Bnip 3介导的线粒体功能障碍与自噬的上调相关。使用模拟I/R和Bnip 3在HL-1心肌细胞中过表达的模型，我们确定Bnip 3介导的自噬活性上调构成了对Bnip 3死亡信号的保护性反应。在这里，我们提出了额外的证据，增强自噬活性的功能作为一种细胞保护途径，以对抗缺血/再灌注相关的细胞凋亡。
Bnip3 is a member of the 'BH3-only' Bd-2 subfamily which has been implicated in apoptotic,(1) necrotic(2) and autophagic cell death.(3,4) We recently reported that Bnip3 is a key mediator of mitochondrial dysfunction and cell death in the ex vivo heart following ischemia/reperfusion (I/R).(5) Moreover, we found that Bnip3 was involved in upregulation of autophagy in I/R and that Bnip3-mediated mitochondrial dysfunction correlated with upregulation of autophagy. Using a model of simulated I/R and overexpression of Bnip3 in HL-1 cardiac myocytes, we determined that Bnip3-mediated upregulation of autophagic activity constituted a protective response against Bnip3 death signaling. Here we present additional evidence that enhanced autophagic activity functions as a cytoprotective pathway to oppose ischemia/reperfusion-related apoptosis.