Mitochondrial adenine nucleotide transport and cardioprotection

Research output: Contribution to journalReview article

Abstract

Mitochondria are highly metabolically active cell organelles that not only act as the powerhouse of the cell by supplying energy through ATP production, but also play a destructive role by initiating cell death pathways. Growing evidence recognizes that mitochondrial dysfunction is one of the major causes of cardiovascular disease. Under de-energized conditions, slowing of adenine nucleotide transport in and out of the mitochondria significantly attenuates myocardial ischemia-reperfusion injury. The purpose of this review is to elaborate on and update the mechanistic pathways which may explain how altered adenine nucleotide transport can influence cardiovascular function. This article is part of a Special Issue entitled "Local Signaling in Myocytes".

Original languageEnglish (US)
Pages (from-to)448-453
Number of pages6
JournalJournal of Molecular and Cellular Cardiology
Volume52
Issue number2
DOIs
StatePublished - Feb 1 2012

Keywords

  • Adenine nucleotide transport
  • Cardioprotection
  • Glycogen Synthase Kinase (GSK)
  • Mitochondria
  • Voltage Dependent Anion Channel (VDAC)

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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