Dear Colleagues,

The pathophysiological mechanisms in cardiomyopathies and the development of heart failure are closely associated with microvascular endothelial inflammation and oxidative stress. It exists both in heart failure with reduced (HFrEF) and preserved ejection fraction (HFpEF). The HFrEF syndrome is primarily driven by neurohormonal activation, and the subsequent development of systemic inflammation is mainly a consequence. In contrast, in HFpEF, the multiplicity of phenotypes suggests a different underlying pathophysiology with comorbidity-driven global inflammation as a disease driver. The multiple co-morbidities result in increased reactive oxygen species (ROS) production and reduced nitric oxide (NO) availability leading to endothelial and microvascular dysfunction causing the stiffening of cardiomyocytes and increased collagen deposition with the development of left ventricular concentric remodeling and mainly diastolic dysfunction.

HFpEF and HFrEF are both associated with abnormal energy metabolism and the increased production of ROS, affecting fatty acid (FA) beta-oxidation. The shift in energy metabolism is a hallmark of heart failure and varies with the progress of the disease. As heart failure develops, FA oxidation, dominating the normal metabolic state in the cardiomyocytes, decreases and glucose metabolism increases, possibly due to impaired mitochondrial function. In end-stage heart failure, insulin resistance develops in the myocardium, glucose oxidation decreases, and ketone bodies and lactate compete as energy substrates, resulting in a shift in energy metabolism regardless of the presence of diabetes.

The role of oxidative stress in the development of cardiomyopathies and energy metabolism in the myocardium is intriguing and may serve as future treatment target. We call colleagues to contribute to this Special Issue, with research findings or literature reviews, where the scope is to explore the role of oxidative stress in cardiomyopathies and the development of cardiac dysfunction.

Dr. Camilla Hage
Guest Editor

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• oxidative stress
• myocardial dysfunction
• microvascular inflammation
• endothelial dysfunction
• mitochondrial dysfunction