Autophagy as a protective response to Bnip3-mediated apoptotic signaling in the heart

被引：95

作者：

Hamacher-Brady, Anne ^{[1
]}

Brady, Nathan R. ^{[1
]}

Gottlieb, Roberta A. ^{[1
]}

Gustafsson, Asa B. ^{[1
]}

机构：

[1] Scripps Res Inst, Dept Mol & Expt Med, La Jolla, CA 92037 USA

来源：

AUTOPHAGY | 2006年 / 2卷 / 04期

关键词：

Bnip3; mitochondria; mitophagy; ischemia/reperfusion; cardiac myocyte;

D O I：

10.4161/auto.2947

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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.

引用

页码：307 / 309

页数：3

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