| dc.description.abstract | In atherosclerosis patients, vascular endothelial dysfunction is commonly
observed alongside damage of the vascular endothelial glycocalyx, an
extracellular matrix bound to and encapsulating the endothelial cells
lining the blood vessel wall. Although atherosclerotic risk factors have
been reported in severe patients with coronavirus disease 2019 (COVID-19),
the exact mechanisms are unclear. The mortality associated with the
COVID-19 outbreak is increased by comorbidities, including hypertension,
diabetes, obesity, chronic obstructive pulmonary disease (COPD), and
cardiovascular disease. Besides, older individuals and smokers have
significantly worse outcomes. Interestingly, these comorbidities and risk
factors are consistent with the pathophysiology that causes vascular
endothelial glycocalyx damage. Moreover, vascular glycocalyx dysfunction
causes microvascular leakage, which results in interstitial pulmonary
abnormal shadows (multiple patchy shadows with a ground glass
inter-pneumonic appearance). This is frequently followed by severe acute
respiratory distress syndrome (ARDS), closely related to
coagulo-fibrinolytic changes contributing to disseminated intravascular coagulation (DIC) and Kawasaki disease shock syndrome, as well as inducing
activation of the coagulation cascade, leading to thromboembolism and
multiple organ failure. Notably, SARS-CoV-2, the causative virus of
COVID-19, binds to ACE2, which is abundantly present not only in human
epithelia of the lung and the small intestine, but also in vascular
endothelial cells and arterial smooth muscle cells. Moreover, COVID-19 can
induce severe septic shock, and sepsis can easily lead to systemic
degradation of the vascular endothelial glycocalyx. In the current review,
we propose new concepts and therapeutic goals for COVID-19-related vascular
endothelial glycocalyx damage, based on previous vascular endothelial
medicine research. | |
