Key result
Myocardial redox imbalance is a hallmark of heart failure, and new therapeutic approaches with antioxidant properties are being developed to modulate ROS and RNS signaling pathways.
This review highlights the complex role of redox imbalance in heart failure and the nuanced potential for targeted antioxidant therapies.
The prevalence of heart failure (HF) is still increasing worldwide, with enormous human, social, and economic costs, in spite of huge efforts in understanding pathogenetic mechanisms and in developing effective therapies that have transformed this syndrome into a chronic disease. Myocardial redox imbalance is a hallmark of this syndrome, since excessive reactive oxygen and nitrogen species can behave as signaling molecules in the pathogenesis of hypertrophy and heart failure, leading to dysregulation of cellular calcium handling, of the contractile machinery, of myocardial energetics and metabolism, and of extracellular matrix deposition. Recently, following new interesting advances in understanding myocardial ROS and RNS signaling pathways, new promising therapeutical approaches with antioxidant properties are being developed, keeping in mind that scavenging ROS and RNS tout court is detrimental as well, since these molecules also play a role in physiological myocardial homeostasis.
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Arcaro et al. (2016) conducted a review in Heart failure. Antioxidant therapies was evaluated. Myocardial redox imbalance is a hallmark of heart failure, and new therapeutic approaches with antioxidant properties are being developed to modulate ROS and RNS signaling pathways.
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