Abstract
Bnip3 is a member of the 'BH3-only' Bcl-2 subfamily which has been implicated in apoptotic, necrotic and autophagic cell death. 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). 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.
Original language | English (US) |
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Pages (from-to) | 307-309 |
Number of pages | 3 |
Journal | Autophagy |
Volume | 2 |
Issue number | 4 |
DOIs | |
State | Published - 2006 |
Externally published | Yes |
Keywords
- Bnip3
- Cardiac myocyte
- Ischemia/reperfusion
- Mitochondria
- Mitophagy
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology