Abstract
Nitric oxide (NO) is a key molecule in cardiovascular homeostasis and its abnormal delivery is highly associated with the occurrence and development of cardiovascular disease (CVD). The assessment and manipulation of NO delivery is crucial to the diagnosis and therapy of CVD, such as endothelial dysfunction, atherosclerotic progression, pulmonary hypertension, and cardiovascular manifestations of coronavirus (COVID-19). However, due to the low concentration and fast reaction characteristics of NO in the cardiovascular system, clinical applications centered on NO delivery are challenging. In this tutorial review, we first summarized the methods to estimate the in vivo NO delivery process, based on computational modeling and flow-mediated dilation, to assess endothelial function and vulnerability of atherosclerotic plaque. Then, emerging bioimaging technologies that have the potential to experimentally measure arterial NO concentration were discussed, including Raman spectroscopy and electrochemical sensors. In addition to diagnostic methods, therapies aimed at controlling NO delivery to regulate CVD were reviewed, including the NO release platform to treat endothelial dysfunction and atherosclerosis and inhaled NO therapy to treat pulmonary hypertension and COVID-19. Two potential methods to improve the effectiveness of existing NO therapy were also discussed, including the combination of NO release platform and computational modeling, and stem cell therapy, which currently remains at the laboratory stage but has clinical potential for the treatment of CVD.
Highlights
Cardiovascular disease (CVD) is a major cause of human morbidity and death [1,2].Nitric oxide (NO) has crucial roles in cardiovascular homeostasis, which occur in a dosedependent manner
This study found that NO concentration is significantly hindered distal to stenosis, which may lead to endothelial dysfunction [32]
The results showed that low NO concentration is related to the occurrence of endothelial dysfunction and high-risk location of atherosclerosis, which is shown in Figure 2a [31]
Summary
Nitric oxide (NO) has crucial roles in cardiovascular homeostasis, which occur in a dosedependent manner. Both high and low local concentrations of NO may induce the development of CVD [3,4]. Is expressed in the endothelium (a single layer of cells that form the lining of blood vessels, of which dysfunction is thought to underpin most types of CVD [5,6,7]), and inducible nitric oxide synthase (iNOS) expressed at the inflammatory site, which mainly catalyze NO formation from L-arginine in the presence of molecular oxygen and reduced nicotinamide adenine dinucleotide phosphate (NADPH) [8]. NO is mainly formed due to the catalysis of eNOS, depending on the mechanotransduction of wall shear stress (WSS) and endothelial function. The subsequent activated cGMP-dependent protein kinases culminate in a decrease in intracellular Ca2+ concentration and the desensitization of the
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