Abstract
Cardiovascular disease (CVD) has been the leading cause of death for many decades, highlighting the importance of new research and treatments in the field. The role of hypoxia and subsequent free radical production [reactive oxygen species (ROS)] have become an area of particular interest in CVD. Interestingly, our laboratory and other laboratories have recently reported positive roles of subcellular ROS in modulating endothelial cell (EC) metabolism, proliferation, and angiogenesis. This bidirectional relationship between ROS and EC metabolism, as well as functional changes, continues to be an area of active research. Interestingly, ECs have been shown to rely on anaerobic processes for ATP generation, despite their direct access to oxygen. This paradox has proven to be beneficial as the major reliance on glycolysis produces ATP faster, preserves oxygen, and results in reduced ROS levels in contrast to oxidative phosphorylation. This review will address the relationship between ROS and carbohydrate, lipid, and nitrogen metabolism in ECs, and their effects on EC phenotype such as sprouting angiogenesis.
Highlights
Cardiovascular diseases (CVDs) are considered to be a major public health burden and a leading cause of global morbidity and mortality (Lozano et al, 2012; Murray et al, 2012)
The complexity of endothelial cell (EC) metabolism is represented by the various mechanisms through which it utilizes carbohydrates, fatty acids, and amino acids as important sources for its energy and nucleotides synthesis
Despite the fact that ECs line the innermost layer of blood vessels and have direct access to oxygen in the blood, ECs rely on anaerobic respiration via glycolysis for over 85% of their energy production (Fitzgerald et al, 2018)
Summary
Cardiovascular diseases (CVDs) are considered to be a major public health burden and a leading cause of global morbidity and mortality (Lozano et al, 2012; Murray et al, 2012). Endothelial cells (ECs) rely on endothelial nitric oxide synthase (eNOS) for its regular function and activity and for the vasculature integrity and homeostasis as a whole. The eNOS activity can be lost or even the enzyme can be uncoupled by oxidative stress (Daiber et al, 2019). Oxidative stress increases the permeability of vascular ECs, promotes the adhesion of leukocyte, and alters EC signal transduction (Lum and Roebuck, 2001; Abid et al, 2007; Lee et al, 2010). Despite the fact that ROS are being generated at injured and inflamed sites, it has been shown that low levels of ROS have an important regulatory role as signaling intermediates that are essential for different cell activities such as cell adaptation and growth (Abid et al, 2000, 2001, 2006, 2007). This review discusses the relationship between ROS with carbohydrate, lipid, and nitrogen metabolism in ECs
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