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Cells
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COVID19, Renin-Angiotensin System and Endothelial Dysfunction
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COVID19, Renin-Angiotensin System and Endothelial Dysfunction

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (30 June 2021) | Viewed by 24240

Special Issue Editor

Prof. Dr. Nader Rahimi

E-Mail Website
Guest Editor
Department of Pathology, Boston University, 670 Albany St. Room 510, Boston, MA 02118, USA
Interests: angiogenesis; vascular biology; cancer biology; cell–cell adhesion; post-translational modifications; signal transduction; endothelial dysfunction; COVID-19
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The newly emergent novel coronavirus disease 2019 (COVID-19) outbreak has posed a serious threat to global public health with major worldwide socio-economic disruption. Now, evidence strongly indicates that mortality with COVID19 is associated with pre-existing conditions such as cardiovascular diseases, diabetes, and hypertension. In light of this, a systematic examination of the molecular basis of SARS-CoV-2 infection, the role of the renin-angiotensin system, in particular, the role angiotensin-converting enzyme 2 (ACE2) and the role of endothelial dysfunction in COVID-19-associated mortality and vice-versa is urgently needed. Understanding the role of the cardiovascular system in SARS-CoV-2 infection is essential to provide medical care for COVID-19 patients with cardiovascular co-morbidity. Moreover, comprehensive knowledge is urgently needed for a mechanistic understanding of the disease and the development of potential therapeutic strategies against COVID-19. This Special Issue of Cells brings together the most recent advances in various aspects of SARS-COV-2, from basic science to applied therapeutic strategies and will provide new insights into our understanding of the role of the cardiovascular system in SARS-CoV-2 infection and how endothelial dysfunction increases COVID-19-associated mortality and whether potential therapeutic strategies could be explored by targeting molecular pathways involved in modulation of endothelial dysfunction.

Prof. Nader Rahimi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • angiotensin-converting enzyme 2 (ACE2)
  • renin-angiotensin system (RAS)
  • cell adhesion molecules
  • peptidases
  • antiviral drugs
  • signal transduction and post-translational modifications
  • endothelial dysfunction
  • hypertension
  • cardiovascular diseases
  • diabetes
  • thrombosis
  • SARS-COV-2
  • SARS-COV

Published Papers (3 papers)

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Review

11 pages, 3978 KiB  
Review
Janus Kinase Signaling Pathway and Its Role in COVID-19 Inflammatory, Vascular, and Thrombotic Manifestations
by Jonathan D. Ravid, Orly Leiva and Vipul C. Chitalia
Cells 2022, 11(2), 306; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11020306 - 17 Jan 2022
Cited by 14 | Viewed by 2281
Abstract
Acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection continues to be a worldwide public health crisis. Among the several severe manifestations of this disease, thrombotic processes drive the catastrophic organ failure and mortality in these patients. In addition to a well-established cytokine storm associated with the [...] Read more.
Acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection continues to be a worldwide public health crisis. Among the several severe manifestations of this disease, thrombotic processes drive the catastrophic organ failure and mortality in these patients. In addition to a well-established cytokine storm associated with the disease, perturbations in platelets, endothelial cells, and the coagulation system are key in triggering systemic coagulopathy, involving both the macro- and microvasculatures of different organs. Of the several mechanisms that might contribute to dysregulation of these cells following SARS-CoV-2 infection, the current review focuses on the role of activated Janus kinase (JAK) signaling in augmenting thrombotic processes and organ dysfunction. The review concludes with presenting the current understanding and emerging controversies concerning the potential therapeutic applications of JAK inhibitors for ameliorating the inflammation-thrombosis phenotype in COVID-19 patients. Full article
(This article belongs to the Special Issue COVID19, Renin-Angiotensin System and Endothelial Dysfunction)
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19 pages, 1332 KiB  
Review
Hyperthrombotic Milieu in COVID-19 Patients
by Mohamed Hassan Kamel, Wenqing Yin, Chris Zavaro, Jean M. Francis and Vipul C. Chitalia
Cells 2020, 9(11), 2392; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9112392 - 31 Oct 2020
Cited by 26 | Viewed by 4325
Abstract
COVID-19 infection has protean systemic manifestations. Experience from previous coronavirus outbreaks, including the current SARS-CoV-2, has shown an augmented risk of thrombosis of both macrovasculature and microvasculature. The former involves both arterial and venous beds manifesting as stroke, acute coronary syndrome and venous [...] Read more.
COVID-19 infection has protean systemic manifestations. Experience from previous coronavirus outbreaks, including the current SARS-CoV-2, has shown an augmented risk of thrombosis of both macrovasculature and microvasculature. The former involves both arterial and venous beds manifesting as stroke, acute coronary syndrome and venous thromboembolic events. The microvascular thrombosis is an underappreciated complication of SARS-CoV-2 infection with profound implications on the development of multisystem organ failure. The telltale signs of perpetual on-going coagulation and fibrinolytic cascades underscore the presence of diffuse endothelial damage in the patients with COVID-19. These parameters serve as strong predictors of mortality. While summarizing the alterations of various components of thrombosis in patients with COVID-19, this review points to the emerging evidence that implicates the prominent role of the extrinsic coagulation cascade in COVID-19-related coagulopathy. These mechanisms are triggered by widespread endothelial cell damage (endotheliopathy), the dominant driver of macro- and micro-vascular thrombosis in these patients. We also summarize other mediators of thrombosis, clinically relevant nuances such as the occurrence of thromboembolic events despite thromboprophylaxis (breakthrough thrombosis), current understanding of systemic anticoagulation therapy and its risk–benefit ratio. We conclude by emphasizing a need to probe COVID-19-specific mechanisms of thrombosis to develop better risk markers and safer therapeutic targets. Full article
(This article belongs to the Special Issue COVID19, Renin-Angiotensin System and Endothelial Dysfunction)
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18 pages, 2866 KiB  
Review
COVID-19, Renin-Angiotensin System and Endothelial Dysfunction
by Razie Amraei and Nader Rahimi
Cells 2020, 9(7), 1652; https://0-doi-org.brum.beds.ac.uk/10.3390/cells9071652 - 09 Jul 2020
Cited by 198 | Viewed by 16676
Abstract
The newly emergent novel coronavirus disease 2019 (COVID-19) outbreak, which is caused by SARS-CoV-2 virus, has posed a serious threat to global public health and caused worldwide social and economic breakdown. Angiotensin-converting enzyme 2 (ACE2) is expressed in human vascular endothelium, respiratory epithelium, [...] Read more.
The newly emergent novel coronavirus disease 2019 (COVID-19) outbreak, which is caused by SARS-CoV-2 virus, has posed a serious threat to global public health and caused worldwide social and economic breakdown. Angiotensin-converting enzyme 2 (ACE2) is expressed in human vascular endothelium, respiratory epithelium, and other cell types, and is thought to be a primary mechanism of SARS-CoV-2 entry and infection. In physiological condition, ACE2 via its carboxypeptidase activity generates angiotensin fragments (Ang 1–9 and Ang 1–7), and plays an essential role in the renin-angiotensin system (RAS), which is a critical regulator of cardiovascular homeostasis. SARS-CoV-2 via its surface spike glycoprotein interacts with ACE2 and invades the host cells. Once inside the host cells, SARS-CoV-2 induces acute respiratory distress syndrome (ARDS), stimulates immune response (i.e., cytokine storm) and vascular damage. SARS-CoV-2 induced endothelial cell injury could exacerbate endothelial dysfunction, which is a hallmark of aging, hypertension, and obesity, leading to further complications. The pathophysiology of endothelial dysfunction and injury offers insights into COVID-19 associated mortality. Here we reviewed the molecular basis of SARS-CoV-2 infection, the roles of ACE2, RAS signaling, and a possible link between the pre-existing endothelial dysfunction and SARS-CoV-2 induced endothelial injury in COVID-19 associated mortality. We also surveyed the roles of cell adhesion molecules (CAMs), including CD209L/L-SIGN and CD209/DC-SIGN in SARS-CoV-2 infection and other related viruses. Understanding the molecular mechanisms of infection, the vascular damage caused by SARS-CoV-2 and pathways involved in the regulation of endothelial dysfunction could lead to new therapeutic strategies against COVID-19. Full article
(This article belongs to the Special Issue COVID19, Renin-Angiotensin System and Endothelial Dysfunction)
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