Oxidative Stress and Inflammation in Heart Failure
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: closed (31 January 2026) | Viewed by 1640
Special Issue Editor
Interests: heart failure; heart failure with preserved ejection fraction; microvascular inflammation; microvascular dysfuncrion; oxidative stress; endothelial dysfunction; proteomics; metabolomics
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The pathophysiological mechanisms underlying cardiomyopathies and the development of heart failure are closely associated with microvascular endothelial inflammation and oxidative stress. These exist both in heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). 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. Multiple comorbidities result in increased reactive oxygen species (ROS) production and reduced nitric oxide (NO) availability, leading to endothelial and microvascular dysfunction, which causes the stiffening of cardiomyocytes and increased collagen deposition, with the development of left-ventricular concentric remodelling and mainly diastolic dysfunction.
HFpEF and HFrEF are both associated with an abnormal energy metabolism and the increased production of ROS, affecting fatty acid (FA) beta-oxidation. A shift in energy metabolism is a hallmark of heart failure and varies with the progression of the disease. As heart failure develops, FA oxidation, dominating the normal metabolic state in 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 represent a future treatment target. We invite you to contribute to this Special Issue with research findings or a literature review. Our aim 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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Keywords
- heart failure
- oxidative stress
- HFrEF
- HFpEF
- reactive oxygen species
- nitric oxide
- cardiomyocytes
- cardiomyopathies
- cardiac dysfunction
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