Abstract
COVID-19 is an endothelial disease. All the major comorbidities that increase the risk for severe SARS-CoV-2 infection and severe COVID-19 including old age, obesity, diabetes, hypertension, respiratory disease, compromised immune system, coronary artery disease or heart failure are associated with dysfunctional endothelium. Genetics and environmental factors (epigenetics) are major risk factors for endothelial dysfunction. Individuals with metabolic syndrome are at increased risk for severe SARS-CoV-2 infection and poor COVID-19 outcomes and higher risk of mortality. Old age is a non-modifiable risk factor. All other risk factors are modifiable. This review also identifies dietary risk factors for endothelial dysfunction. Potential dietary preventions that address endothelial dysfunction and its sequelae may have an important role in preventing SARS-CoV-2 infection severity and are key factors for future research to address. This review presents some dietary bioactives with demonstrated efficacy against dysfunctional endothelial cells. This review also covers dietary bioactives with efficacy against SARS-CoV-2 infection. Dietary bioactive compounds that prevent endothelial dysfunction and its sequelae, especially in the gastrointestinal tract, will result in more effective prevention of SARS-CoV-2 variant infection severity and are key factors for future food research to address.
Highlights
COVID-19 is an endothelial disease associated with endothelial dysfunction, which has been recognized as crucial in the pathogenesis and progression of COVID-19 [1–4]
SARS-CoV-2-and COVID-19-associated dysfunctional endothelium is characterized by dysregulation and disruption of endothelial homeostasis toward a pro-inflammatory phenotype, hyperproduction of inflammatory cytokines including IL-6, IL-8, and TNF-α and dysregulation of coagulation, vascular tone, endothelial permeability, and vascular inflammation
Oxidative stress may be generated by several pathological conditions such as hyperglycemia, diabetes, hypertension, dyslipidemia, smoking, or high levels of oxidized low-density lipoproteins; all these factors are able to produce reactive oxygen species (ROS), which in turn rapidly inactivate nitric oxide (NO) [39,40]
Summary
Endothelial dysfunction is synonymous with altered endothelial cell phenotype in which the reduced production and bioavailability of NO promote a pro-thrombotic and pro-inflammatory state [16]. The decline in NO bioavailability disrupts the physiological homeostasis of the vessel wall and favors the increased, unbalanced bioactivity of vasoconstrictor and pro-atherogenic factors such as ET-1. This predisposes the vessels to leukocyte adhesion, platelet activation, oxidative stress, thrombosis, coagulation, and inflammation, promoting the formation and progression of atherogenic plaques [17,18]. Endothelial dysfunction increases the permeability of endothelium to lipoproteins, monocytes, and macrophages, enhancing smooth muscle cell migration and proliferation and aiding the formation of an intermediate lesion and progression to atherosclerotic plaques [23,24]. The presence of endothelial abnormalities in old people becomes a risk factor for the pathogenesis of cardiovascular disease, including atherosclerosis and hypertension [28,29], endothelial dysfunction is a risk factor for aging-related diseases such as erectile dysfunction, renal failure, circadian cycle alterations, osteoporosis, retinopathy, and Alzheimer’s disease [30–35]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
