Mitochondrial dysfunction and oxidative damage to sarcomeric proteins

Marina Bayeva, Hossein Ardehali*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

41 Scopus citations

Abstract

Hypertension is an important risk factor for the development of heart failure. Increased production of reactive oxygen species (ROS) contributes to cardiac dysfunction by activating numerous pro-hypertrophic signaling cascades and damaging the mitochondria, thus setting off a vicious cycle of ROS generation. The way in which oxidative stress leads to exacerbation of systolic and diastolic dysfunction is still unclear, however. In skeletal muscle and ischemic myocardium, increased ROS production causes preferential oxidation of myofibrillar proteins and provides a mechanistic link between oxidative damage and impaired contractility through disruption of actin-myosin interactions, enzymatic functions, calcium sensitivity, and efficiency of cross-bridge cycling. In this review, we summarize recent findings in the fields of heart failure and sarcomere biology and speculate that oxidative damage to myofibrils may contribute to the development of heart failure.

Original languageEnglish (US)
Pages (from-to)426-432
Number of pages7
JournalCurrent Hypertension Reports
Volume12
Issue number6
DOIs
StatePublished - Dec 1 2010

Keywords

  • Contractile dysfunction
  • Diastolic dysfunction
  • Heart failure
  • Hypertension
  • Hypertrophy
  • Mitochondria
  • Myofibrils
  • ROS
  • Sarcomere

ASJC Scopus subject areas

  • Internal Medicine

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