Nix Nought Nothing: Fairy tale or real deal

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Abstract

Nix was first described in the heart as the protein product of a differentially expressed mRNA detected by hybridization to a partial cDNA sequence tag on an RNA expression array. Over the subsequent 8. years Nix has become the prototypical transcriptionally-regulated cardiac myocyte "suicide" gene and has been used as a model to interrogate mechanisms of programmed cardiomyocyte death in hypertrophy and heart failure. Nix stimulates conventional apoptosis mediated via the intrinsic mitochondrial pathway, but emerging evidence indicates that Nix also controls programmed necrosis dependent upon sarcoplasmic reticular-mitochondrial tethering, calcium cross-talk, and the mitochondrial permeability transition. Recent studies have also described Nix labeling of senescent cardiomyocyte mitochondria for autophagic elimination, elucidated a physiological mitochondrial quality control Nix function; so-called "mitochondrial pruning". This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure.".

Original languageEnglish
Pages (from-to)497-500
Number of pages4
JournalJournal of Molecular and Cellular Cardiology
Volume51
Issue number4
DOIs
StatePublished - Oct 2011

Keywords

  • Apoptosis
  • Autophagy
  • Heart failure
  • Programmed necrosis

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