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

Anne Hamacher-Brady, Nathan R. Brady, Roberta A. Gottlieb, Åsa B. Gustafsson

Research output: Contribution to journalArticle

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 languageEnglish (US)
Pages (from-to)307-309
Number of pages3
JournalAutophagy
Volume2
Issue number4
DOIs
StatePublished - Jan 1 2006
Externally publishedYes

Keywords

  • Bnip3
  • Cardiac myocyte
  • Ischemia/reperfusion
  • Mitochondria
  • Mitophagy

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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