Role of Oxidative Stress in Subcellular Defects in Ischemic Heart Disease

  • Monika Bartekova
  • Miroslav Barancik
  • Naranjan S. DhallaEmail author
Part of the Advances in Biochemistry in Health and Disease book series (ABHD, volume 16)


Ischemic heart disease is caused by obstruction of the coronary arteries that reduces myocardial perfusion. The most efficient way to restore blood supply to the ischemic myocardium is reperfusion of the affected area. However, if reperfusion is initiated too late, it enhances ischemia-reperfusion damage to the heart. Oxidative stress is one of the major causes for the development of ischemia-reperfusion (I/R) injury to the heart, which is characterized by decreased functional performance, ultrastructural changes and metabolic alterations. Excessive formation of oxyradicals during the development of I/R injury has now been shown to produce a wide variety of abnormalities in cardiac subcellular organelles such as sarcolemma, sarcoplasmic reticulum, mitochondria and myofibrils. Different reactive oxygen species (ROS) have been shown to cause alterations in several proteins leading to their malfunction and changes in enzyme activities. Lipid peroxidation leads to depressed membrane fluidity and increased permeability, as well as changes in gene expression leading to impaired recovery of cardiac dysfunction due to I/R injury. Since the redox status of cardiomyocytes depends mainly on the balance between ROS production and availability of endogenous antioxidant defense systems, extensive efforts are made to maintain the redox status during I/R injury. Cardioprotection by ischemic conditioning as well as treatment of the heart with exogenous antioxidants have been observed to result in the increased availability of endogenous antioxidants and prevent oxidative damage to subcellular organelles. Thus antioxidant therapy is considered to be a promising strategy to decrease the I/R induced damage to the heart. Accordingly, this article is intended to describe the mechanisms of oxidative stress induced subcellular defects leading to cardiac dysfunction due to I/R injury and to outline the role of antioxidant defense mechanisms in the prevention as well as treatment of the ischemic heart disease.


Oxyradicals Iintracellular Ca2+-overload Antioxidants Oxidative stress Subcellular abnormalities Cardiac dysfunction Ischemia-reperfusion injury Lipid peroxidation Proteolysis 


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Copyright information

© Springer International Publishing Switzerland 2016

Authors and Affiliations

  • Monika Bartekova
    • 1
  • Miroslav Barancik
    • 1
  • Naranjan S. Dhalla
    • 2
    Email author
  1. 1.Institute for Heart ResearchSlovak Academy of SciencesBratislavaSlovak Republic
  2. 2.Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Department of Physiology and Pathophysiology, Max Rady College of MedicineUniversity of ManitobaWinnipegCanada

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