Iron-Induced Damage in Cardiomyopathy: Oxidative-Dependent and Independent Mechanisms

Figure 1

Roles of iron in the pathologic progression leading to cardiac dysfunction. Excess iron, derived from either systemic overload (e.g., in thalassemia) or mislocalization (e.g., in FRDA), can directly catalyze ROS formation. Alternatively, iron may function as cofactor of other damaging agents, such as the cardiotoxic drug doxorubicin, or events, like postischemic reperfusion, and amplify their oxidative-dependent cardiotoxic effect. As described in the text, iron may also influence inflammatory events and repair processes, thereby fueling the progression of cardiomyopathy. The possible therapeutic interventions are also highlighted.