Vascular Endothelial Glycocalyx Damage in COVID-19

Yamaoka‐Tojo, Minako

doi:10.3390/ijms21249712

Cited by 71 publications

(86 citation statements)

References 91 publications

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“…The endothelial dysfunction associated with COVID-19 [20] may also be a contributing factor for PRES and other vascular complications (e.g., myocardial infarction and ischemic stroke). Recent pre-clinical and autopsy studies support this hypothesis, as alterations of the microcirculation and vascular endothelial glycocalyx have been detected in patients with severe COVID-19 [21,22]. The absence of severe hypertension in most patients in this case series, coupled with the significant level of systemic inflammation would support this theory.…”

Section: Discussionsupporting

confidence: 64%

Posterior reversible encephalopathy syndrome (PRES) associated with COVID-19

Lallana

Chen

Requena

et al. 2021

Journal of Clinical Neuroscience

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The novel human coronavirus disease (COVID-19) has been associated with vascular and thrombotic complications, some of which may result from endothelial dysfunction, including the posterior reversible encephalopathy syndrome (PRES). We report a case series of 8 patients with COVID-19 and PRES diagnosed at two academic medical centers between March and July of 2020. The clinical, laboratory and radiographic data, treatment, and short-term outcomes were retrospectively analyzed. The mean age was 57.9 ± 12 years, and 50% were women. Four patients had previous vascular comorbidities. All the patients suffered from severe pneumonia, requiring intensive care unit admission. Five patients were not hypertensive at presentation (all SBP < 127 mmHg). Neurologic symptoms included seizures in 7 patients; impaired consciousness in 5 patients; focal neurological signs in 3 patients; and visual disturbances in 1 patient. All patients underwent brain magnetic resonance imaging which indicated asymmetric T2 prolongation or diffusion changes (50%), extensive fronto-parieto-occipital involvement (25%), vascular irregularities (12.5%) and intracranial hemorrhage (25%). Four patients were treated with tocilizumab. Three patients were discharged without neurologic disability, 2 patients had persistent focal neurologic deficits and 2 expired. One patient's prognosis remains guarded. Together, these data support the relationship between PRES and endothelial dysfunction associated with severe COVID-19. In patients with severe COVID-19, PRES can be triggered by uncontrolled hypertension, or occur independently in the setting of systemic illness and certain medications. Like other infectious processes, critically ill patients with COVID-19 may be at greater risk of PRES because of impaired vasoreactivity or the use of novel agents like Tocilizumab.

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Section: Discussionsupporting

confidence: 64%

Posterior reversible encephalopathy syndrome (PRES) associated with COVID-19

Lallana

Chen

Requena

et al. 2021

Journal of Clinical Neuroscience

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“…Under the condition of old age and/or comorbidities, including chronic obstructive pulmonary disease, hypertension, cardiovascular disease, diabetes, and obesity, damage of the vascular endothelial glycocalyx has been associated with poor prognosis in severe COVID-19 patients [ 158 ]. The glycocalyx is a gel-like layer covering the surface of all living cells; it is composed of a membrane-binding domain consisting of sialic acid-containing glycoproteins, syndecans, HS, and hyaluronic acid (HA).…”

Section: Heparan Sulfate Proteoglycan Involvement In the Pathogenicity Of Sars-cov-2mentioning

confidence: 99%

Heparan Sulfate Proteoglycans in Viral Infection and Treatment: A Special Focus on SARS-CoV-2

Pasquale

Quiccione

Tafuri

et al. 2021

IJMS

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Heparan sulfate proteoglycans (HSPGs) encompass a group of glycoproteins composed of unbranched negatively charged heparan sulfate (HS) chains covalently attached to a core protein. The complex HSPG biosynthetic machinery generates an extraordinary structural variety of HS chains that enable them to bind a plethora of ligands, including growth factors, morphogens, cytokines, chemokines, enzymes, matrix proteins, and bacterial and viral pathogens. These interactions translate into key regulatory activity of HSPGs on a wide range of cellular processes such as receptor activation and signaling, cytoskeleton assembly, extracellular matrix remodeling, endocytosis, cell-cell crosstalk, and others. Due to their ubiquitous expression within tissues and their large functional repertoire, HSPGs are involved in many physiopathological processes; thus, they have emerged as valuable targets for the therapy of many human diseases. Among their functions, HSPGs assist many viruses in invading host cells at various steps of their life cycle. Viruses utilize HSPGs for the attachment to the host cell, internalization, intracellular trafficking, egress, and spread. Recently, HSPG involvement in the pathogenesis of SARS-CoV-2 infection has been established. Here, we summarize the current knowledge on the molecular mechanisms underlying HSPG/SARS-CoV-2 interaction and downstream effects, and we provide an overview of the HSPG-based therapeutic strategies that could be used to combat such a fearsome virus.

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“…Immune cells, including monocytes and neutrophils; inflammatory cytokines, such as IL-1β, TNF, IL-6, and IL-8; and vasoactive molecules, such as thrombin, histamine, bradykinin, thromboxane A 2 , and vascular endothelial growth factor (VEGF), cause loosening of inter-endothelial junctions and enhancement of endothelial cell contractility, which pulls endothelial cells apart, leading to inter-endothelial gaps [ 13 ]. The glycocalyx is a gel-like layer that covers the surface of endothelial cells and plays a crucial role in the regulation of vascular permeability [ 76 ]. Cytokines, including IL-1β and TNF, upregulate glucuronidases that degrade the glycocalyx, leading to increased vascular permeability.…”

Section: Endothelial Dysfunction In the Lungmentioning

confidence: 99%

Pathophysiological Association of Endothelial Dysfunction with Fatal Outcome in COVID-19

Maruhashi

Higashi

2021

IJMS

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The outbreak of coronavirus disease 2019 (COVID-19) caused by the betacoronavirus SARS-CoV-2 is now a worldwide challenge for healthcare systems. Although the leading cause of mortality in patients with COVID-19 is hypoxic respiratory failure due to viral pneumonia and acute respiratory distress syndrome, accumulating evidence has shown that the risk of thromboembolism is substantially high in patients with severe COVID-19 and that a thromboembolic event is another major complication contributing to the high morbidity and mortality in patients with COVID-19. Endothelial dysfunction is emerging as one of the main contributors to the pathogenesis of thromboembolic events in COVID-19. Endothelial dysfunction is usually referred to as reduced nitric oxide bioavailability. However, failures of the endothelium to control coagulation, inflammation, or permeability are also instances of endothelial dysfunction. Recent studies have indicated the possibility that SARS-CoV-2 can directly infect endothelial cells via the angiotensin-converting enzyme 2 pathway and that endothelial dysfunction caused by direct virus infection of endothelial cells may contribute to thrombotic complications and severe disease outcomes in patients with COVID-19. In this review, we summarize the current understanding of relationships between SARS-CoV-2 infection, endothelial dysfunction, and pulmonary and extrapulmonary complications in patients with COVID-19.

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Vascular Endothelial Glycocalyx Damage in COVID-19

Cited by 71 publications

References 91 publications

Posterior reversible encephalopathy syndrome (PRES) associated with COVID-19

Posterior reversible encephalopathy syndrome (PRES) associated with COVID-19

Heparan Sulfate Proteoglycans in Viral Infection and Treatment: A Special Focus on SARS-CoV-2

Pathophysiological Association of Endothelial Dysfunction with Fatal Outcome in COVID-19

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