Mitochondria: A mirror into cellular dysfunction in heart disease

Melanie Y. White, Alistair V.G. Edwards, Stuart J. Cordwell, Jennifer E. Van Eyk

Research output: Contribution to journalReview articlepeer-review

26 Scopus citations


Cardiovascular (CV) disease is the single most significant cause of morbidity and mortality worldwide. The emerging global impact of CV disease means that the goals of early diagnosis and a wider range of treatment options are now increasingly pertinent. As such, there is a greater need to understand the molecular mechanisms involved and potential targets for intervention. Mitochondrial function is important for physiological maintenance of the cell, and when this function is altered, the cell can begin to suffer. Given the broad range and significant impacts of the cellular processes regulated by the mitochondria, it becomes important to understand the roles of the proteins associated with this organelle. Proteomic investigations of the mitochondria are hampered by the intrinsic properties of the organelle, including hydrophobic mitochondrial membranes; high proportion of basic proteins (pI greater than 8.0); and the relative dynamic range issues of the mitochondria. For these reasons, many proteomic studies investigate the mitochondria as a discrete subproteome. Once this has been achieved, the alterations that result in functional changes with CV disease can be observed. Those alterations that lead to changes in mitochondrial function, signaling and morphology, which have significant implications for the cardiomyocyte in the development of CV disease, are discussed.

Original languageEnglish (US)
Pages (from-to)845-861
Number of pages17
JournalProteomics - Clinical Applications
Issue number6
StatePublished - Jun 2008
Externally publishedYes


  • Cardiovascular disease
  • Complex 1
  • Mitochondria
  • Oxidative phosphorylation
  • Reactive oxygen species

ASJC Scopus subject areas

  • Clinical Biochemistry


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