Effects of axial stretch on mitochondrial reactive oxygen species in cardiac myocytes

Gentaro Iribe, Keiko Kaihara, Keiji Naruse

Research output: Contribution to journalArticlepeer-review


Myocardium contracts against ventricular wall stretch that comes along with ventricular filling. Mitochondria generate required ATP for myocardial contraction. It is well known that mitochondrial ATP production process is one of the sources of reactive oxygen species (ROS). ROS are known as toxic molecules, but also important physiological regulators of intracellular signaling pathways. In the present study, we investigate the relation between myocardial stretch and mitochondrial ROS production, and discuss the role of mitochondria on myocardial response to stretch. Isolated mouse ventricular myocytes were exposed to 10% axial stretch using carbon fiber technique. ROS production was studied using DCF-loaded cells. Axial stretch significantly increased ROS production. Applying 5 μM mitochondrial metabolic uncoupler FCCP blunted the response, indicating mitochondrial ROS production is stretch-sensitive. The present results suggest that stretch enhances electron transport chain to prepare for the more ATP production for the more preloaded, namely, the more energy-consuming contraction.

Original languageEnglish
Pages (from-to)SY-44
JournalTransactions of Japanese Society for Medical and Biological Engineering
Publication statusPublished - Aug 17 2014


  • Biomechanics
  • Mechano-electric coupling
  • Stretch

ASJC Scopus subject areas

  • Biomedical Engineering


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