New aspects of impaired mitochondrial function in heart failure

Mariana G. Rosca, Charles L. Hoppel

Research output: Contribution to journalShort surveypeer-review

44 Scopus citations


This minireview focuses on the impairment of function in cardiac mitochondria in heart failure (HF). It is generally accepted that chronic energy starvation leads to cardiac mechanical dysfunction in HF. Mitochondria are the primary ATP generator for the heart. Current evidence suggests that the assembly of the electron transport chain (ETC) into respirasomes provides structural support for mitochondrial oxidative phosphorylation by facilitating electron channeling and perhaps by preventing electron leak and superoxide production. Defects have been purported to occur in the individual ETC complexes or components of the phosphorylation apparatus in HF, but these defects have not been linked to impaired mitochondrial function. Moreover, studies that reported decreased mitochondrial oxidative phosphorylation in HF did not identify the site of the defect. We propose a sequential mechanistic pathway in which the decrease in functional respirasomes in HF is the primary event causing decreased oxidative phosphorylation and increased reactive oxygen species production, leading to a progressive decrease in cardiac performance.

Original languageEnglish
Pages (from-to)107-112
Number of pages6
JournalJournal of Bioenergetics and Biomembranes
Issue number2
StatePublished - Apr 2009


  • Heart failure
  • Mitochondria
  • Oxidative phosphorylation
  • Respirasomes


Dive into the research topics of 'New aspects of impaired mitochondrial function in heart failure'. Together they form a unique fingerprint.

Cite this