Mitochondrial protein phosphorylation as a regulatory modality: Implications for mitochondrial dysfunction in heart failure

Brian O'Rourke, Jennifer E. van Eyk, D. Brian Foster

Research output: Contribution to journalReview articlepeer-review

Abstract

Phosphorylation of mitochondrial proteins has been recognized for decades, and the regulation of pyruvate- and branched-chain α-ketoacid dehydrogenases by an atypical kinase/phosphatase cascade is well established. More recently, the development of new mass spectrometry-based technologies has led to the discovery of many novel phosphorylation sites on a variety of mitochondrial targets. The evidence suggests that the major classes of kinase and several phosphatases may be present at the mitochondrial outer membrane, intermembrane space, inner membrane, and matrix, but many questions remain to be answered as to the location, timing, and reversibility of these phosphorylation events and whether they are functionally relevant. The authors review phosphorylation as a mitochondrial regulatory strategy and highlight its possible role in the pathophysiology of cardiac hypertrophy and failure.

Original languageEnglish (US)
Pages (from-to)269-282
Number of pages14
JournalCongestive Heart Failure
Volume17
Issue number6
DOIs
StatePublished - Nov 2011

ASJC Scopus subject areas

  • Emergency Medicine
  • Emergency
  • Cardiology and Cardiovascular Medicine

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