SARS-CoV-2 and endothelial cell interaction in COVID-19: molecular perspectives

Giordo, Roberta; Paliogiannis, Panagiotis; Mangoni, Arduino A.; Pintus, Gianfranco

doi:10.1530/vb-20-0017

Cited by 34 publications

(30 citation statements)

References 71 publications

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“…COVID-19-associated coagulopathy is characterized by some unique features that are at least in part driven by the direct interaction between the causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and endothelial cells [ 3 ]. As a result, the endothelial von Willebrand factor (VWF) and angiopoietin 2 are released into the circulation with consequent platelet activation and aggregation and stimulation of pro-inflammatory pathways [ 57 , 58 ].…”

Section: Discussionmentioning

confidence: 99%

“…Coronavirus disease 2019 (COVID-19) is frequently characterized by the presence of significant coagulopathy, particularly in the setting of a systemic release of pro-inflammatory and pro-oxidant cytokines and multi-organ compromise [ 1 ]. The COVID-19-associated coagulopathy typically involves the combined activation of coagulation, immune, and complement pathways and endothelial dysfunction [ 2 , 3 ]. This process results in the formation of thrombi both in the large vessels and in the microvasculature of the lungs and other organs, resembling disseminated intravascular coagulation (DIC) [ 2 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

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INR and COVID-19 severity and mortality: A systematic review with meta-analysis and meta-regression

Zinellu

Paliogiannis

Carru

et al. 2021

Advances in Medical Sciences

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Objectives D-dimer elevations, suggesting a pro-thrombotic state and coagulopathy, predict adverse outcomes in coronavirus disease 2019 (COVID-19). However, the clinical significance of other coagulation markers, particularly the international normalized ratio (INR), is not well established. We conducted a systematic review and meta-analysis of the INR in COVID-19. Methods A literature search was conducted in PubMed, Web of Science and Scopus, between January 2020 and February 2021, for studies reporting INR values, measures of COVID-19 severity, and mortality (PROSPERO registration number: CRD42021241468). Results Thirty-eight studies in 7,440 COVID-19 patients with low disease severity or survivor status during follow up (50% males, mean age 57 years) and 2,331 with high severity or non-survivor status (60% males, mean age 69 years) were identified. The INR was significantly prolonged in patients with severe disease or non-survivor status than in patients with mild disease or survivor status (standard mean difference, SMD, 0.60; 95% confidence interval, CI 0.42 to 0.77; p<0.001). There was extreme between-study heterogeneity (I 2 =90.2%; p<0.001). Sensitivity analysis, performed by sequentially removing each study and re-assessing the pooled estimates, showed that the magnitude and direction of the effect size was not modified. The Begg's and Egger's t-tests did not show publication bias. In meta-regression, the SMD of the INR was significantly associated with C-reactive protein (p=0.048) and D-dimer (p=0.001). Conclusions Prolonged INR values were significantly associated with COVID-19 severity and mortality. Both INR prolongation and D-dimer elevations can be useful in diagnosing COVID-19-associated coagulopathy and predicting clinical outcomes.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

INR and COVID-19 severity and mortality: A systematic review with meta-analysis and meta-regression

Zinellu

Paliogiannis

Carru

et al. 2021

Advances in Medical Sciences

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“…These symptoms appear to arise from pathophysiologic changes that span many organ systems and tissues, potentially explained by SARS-CoV-2's interaction with the endothelium. 15 Given the timeline of SARS-CoV-2's emergence, studies to date have tracked patients' clinical course up to six months post-infection, [16][17][18] but anecdotal reports are available describing patients with ongoing symptoms as long as one year post-infection. 19 Symptoms experienced after the acute illness represent a significant challenge for patients, physicians, and society as a whole.…”

Section: Clinical Presentationmentioning

confidence: 99%

Characterizing Long COVID: Deep Phenotype of a Complex Condition

Deer

Liu

Haendel

et al. 2021

Preprint

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Importance: Since late 2019, the novel coronavirus SARS-CoV-2 has given rise to a global pandemic and introduced many health challenges with economic, social, and political consequences. In addition to a complex acute presentation that can affect multiple organ systems, there is mounting evidence of various persistent long-term sequelae. The worldwide scientific community is characterizing a diverse range of seemingly common long-term outcomes associated with SARS-CoV-2 infection, but the underlying assumptions in these studies vary widely making comparisons difficult. Numerous publications describe the clinical manifestations of post-acute sequelae of SARS-CoV-2 infection (PASC or long COVID), but they are difficult to integrate because of heterogeneous methods and the lack of a standard for denoting the many phenotypic manifestations of long COVID. Observations: We identified 303 articles published before April 29, 2021, curated 59 relevant manuscripts that described clinical manifestations in 81 cohorts of individuals three weeks or more following acute COVID-19, and mapped 287 unique clinical findings to Human Phenotype Ontology (HPO) terms. Conclusions and Relevance: Patients and clinicians often use different terms to describe the same symptom or condition. Addressing the heterogeneous and inconsistent language used to describe the clinical manifestations of long COVID combined with the lack of standardized terminologies for long COVID will provide a necessary foundation for comparison and meta-analysis of different studies. Translating long COVID manifestations into computable HPO terms will improve the analysis, data capture, and classification of long COVID patients. If researchers, clinicians, and patients share a common language, then studies can be compared or pooled more effectively. Furthermore, mapping lay terminology to HPO for long COVID manifestations will help patients assist clinicians and researchers in creating phenotypic characterizations that are computationally accessible, which may improve the stratification and thereby diagnosis and treatment of long COVID.

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“…Likewise, extensive research is being focused on EC dysfunction following SARS-CoV-2 infection. It has been demonstrated that neuropillin-1 positive endothelial cells of small and medium-sized vessels were infected with SARS-CoV-2 [ 140 ]. Case reports have shown direct invasion of the SARS-CoV-2 virus into ECs, leading to EC activation and apoptosis as well as pyroptosis [ 97 , 141 ].…”

Section: Sars-cov-2 and Its Receptors In Blood Vessel Pathophysiologymentioning

confidence: 99%

The SARS-CoV-2/Receptor Axis in Heart and Blood Vessels: A Crisp Update on COVID-19 Disease with Cardiovascular Complications

Veluswamy

Wacker

Stavridis

et al. 2021

Viruses

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The SARS-CoV-2 virus causing COVID-19 disease has emerged expeditiously in the world and has been declared pandemic since March 2020, by World Health Organization (WHO). The destructive effects of SARS-CoV-2 infection are increased among the patients with pre-existing chronic conditions and, in particular, this review focuses on patients with underlying cardiovascular complications. The expression pattern and potential functions of SARS-CoV-2 binding receptors and the attributes of SARS-CoV-2 virus tropism in a physio-pathological state of heart and blood vessel are precisely described. Of note, the atheroprotective role of ACE2 receptors is reviewed. A detailed description of the possible detrimental role of SARS-CoV-2 infection in terms of vascular leakage, including endothelial glycocalyx dysfunction and bradykinin 1 receptor stimulation is concisely stated. Furthermore, the potential molecular mechanisms underlying SARS-CoV-2 induced clot formation in association with host defense components, including activation of FXIIa, complements and platelets, endothelial dysfunction, immune cell responses with cytokine-mediated action are well elaborated. Moreover, a brief clinical update on patient with COVID-19 disease with underlying cardiovascular complications and those who had new onset of cardiovascular complications post-COVID-19 disease was also discussed. Taken together, this review provides an overview of the mechanistic aspects of SARS-CoV-2 induced devastating effects, in vital organs such as the heart and vessels.

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SARS-CoV-2 and endothelial cell interaction in COVID-19: molecular perspectives

Cited by 34 publications

References 71 publications

INR and COVID-19 severity and mortality: A systematic review with meta-analysis and meta-regression

INR and COVID-19 severity and mortality: A systematic review with meta-analysis and meta-regression

Characterizing Long COVID: Deep Phenotype of a Complex Condition

The SARS-CoV-2/Receptor Axis in Heart and Blood Vessels: A Crisp Update on COVID-19 Disease with Cardiovascular Complications

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