The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited

Figure 2

This schematic illustration describes the central role of reductive stress in modulating the myocardial tissue injury. Under normal oxidative stress condition, activation of Nrf-2 results in augmenting endogenous defense system, which aids in the resolution of the tissue injury. However, during sustained oxidative stress condition, Nrf-2 is profoundly activated, which results in the production of increased reducing equivalents such as GSH, which then indulges in posttranslational modification of critical proteins in cardiomyocyte function, whereby affecting their structure and function. These phenotypic events culminate in defective autophagy and drive the cardiomyocytes to become hypertrophic, producing extracellular matrix and committing suicide (apoptosis). All these phenotypic events collectively contribute to the pathogenesis of heart failure. Glutamate-cysteine ligase modifier subunit (GCLm); glutamate-cysteine ligase catalytic subunit (GCLc).