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Sars-Cov-2 Cell Entry Receptor Ace2 Mediated Endothelial Dysfunction Leads to Vascular Thrombosis in COVID-19 Patients

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TLDR
This work proposes a SARS-CoV-2 cell entry receptor ACE2 based mechanism for vascular thrombosis in COVID-19 patients, which is based on the circumstantial evidence present in the literature.
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This article is published in Medical Hypotheses.The article was published on 2020-09-30 and is currently open access. It has received 49 citations till now. The article focuses on the topics: Endothelial dysfunction & Angiotensin-converting enzyme 2.

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Endothelial Damage in Acute Respiratory Distress Syndrome.

TL;DR: The underlying pathology of endothelial dysfunction leading to ARDS and emerging therapies are discussed, and it is presented that endotheliopathy is an important feature of hospitalised patients with coronavirus disease-19 (COVID-19).
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SARS-CoV-2 Spike Protein Disrupts Blood-Brain Barrier Integrity via RhoA Activation.

TL;DR: In this article, a 3D-BBB microfluidic model was used to interrogate mechanisms by which the spike protein may facilitate barrier dysfunction, but its pathogenic mechanism of action is unknown.
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Therapeutic Potential of Metformin in COVID-19: Reasoning for Its Protective Role.

TL;DR: In this article, the authors discuss the multifaceted ability of metformin to control blood glucose levels and possibly attenuate endothelial dysfunction, inhibit viral entry and infection, and modify inflammatory and immune responses during SARS-CoV-2 infections.
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The Contribution of Endothelial Dysfunction in Systemic Injury Subsequent to SARS-Cov-2 Infection.

TL;DR: The review aims to assess some recent advances to define the crucial role of endothelial dysfunction in the pathogenesis of vascular complications accompanying SARS-CoV-2 infection and the molecular mechanisms associated with the interaction with the ACE2 receptor located on the endothelial cells are highlighted to support its role in compromising endothelial cell functionality.
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COVID-19 Mechanisms in the Human Body-What We Know So Far.

TL;DR: A review of the progress made since the commencement of the COVID-19 pandemic can be found in this article, where the authors narrate the progress in the human body, including virus-host interactions, pulmonary and other systemic manifestations, immunological dysregulations, complications, host-specific vulnerability, and long-term health consequences in the survivors.
References
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Journal ArticleDOI

Endothelial cell infection and endotheliitis in COVID-19.

TL;DR: The vascular endothelium is an active paracrine, endocrine, and Endothelial cell infection and endotheliitis in COVID-19 and recruitment of immune cells can result in widespread endothelial dysfunction associated with apoptosis.
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Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia.

TL;DR: In the recent outbreak of novel coronavirus infection in Wuhan, China, significantly abnormal coagulation parameters in severe novel coronvirus pneumonia (NCP) cases were a concern.
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Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19.

TL;DR: In this small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection.
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Incidence of thrombotic complications in critically ill ICU patients with COVID-19.

TL;DR: The findings reinforce the recommendation to strictly apply pharmacological thrombosis prophylaxis in all COVID-19 patients admitted to the ICU, and are strongly suggestive of increasing the prophYLaxis towards high-prophylactic doses, even in the absence of randomized evidence.
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