scholarly journals COVID-19, Renin-Angiotensin System and Endothelial Dysfunction

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1652 ◽  
Author(s):  
Razie Amraei ◽  
Nader Rahimi
Keyword(s):  
Endothelial Dysfunction ◽  
Molecular Mechanisms ◽  
Cell Injury ◽  
Renin Angiotensin System ◽  
Vascular Damage ◽  
Host Cells ◽  
Ras Signaling ◽  
Global Public Health ◽  
Angiotensin System ◽  
Renin Angiotensin

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.

The Therapeutic Potential of Targeting the Angiotensin Pathway as a Novel Therapeutic Approach to Ameliorating Post-Surgical Adhesions

2021 ◽  
Vol 27 ◽  
Author(s):  
Ghazaleh Khalili-Tanha ◽  
Nima Khalili-Tanha ◽  
Seyedeh Elnaz Nazari ◽  
Negin Chaeichi-Tehrani ◽  
Majid Khazaei ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Healing Process ◽  
Adhesion Formation ◽  
Surgical Techniques ◽  
Renin Angiotensin System ◽  
Cochrane Library ◽  
Ras Signaling ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Surgical Adhesions

Background: Post-surgical adhesion is a common complication after abdominal or pelvic surgeries. Despite improvements in surgical techniques or the application of physical barriers, little improvements have been achieved. It causes bowel obstruction, pelvic pain, and infertility in women and has an adverse effect on the quality of life. Renin-Angiotensin System (RAS) is traditionally considered as a blood pressure regulator. However, recent studies also indicate that the RAS plays a vital role in other processes, including oxidative stress, fibrosis, proliferation, inflammation, and the wound healing process. Angiotensin II (Ang II) is the main upstream effector of the RAS that can bind to the AT1 receptor (ATIR). A growing body of evidence has revealed that targeting Angiotensin-Converting Enzyme Inhibitors (ACEIs), Angiotensin II type 1 Receptor Blockers (ARBs), and Direct Renin Inhibitors (DRIs) can prevent post-surgical adhesions. Here we provide an overview of the therapeutic effect of RAS antagonists for adhesion. Methods: PubMed, EMBASE, and the Cochrane library were reviewed to identify potential agents targeting the RAS system as a potential approach for post-surgical adhesion. Results: Available evidence suggests the involvement of the RAS signaling pathway in inflammation, proliferation, and fibrosis pathways as well as in post-surgical adhesions. Several FDA-approved drugs are being used for targeting the RAS system. Some of them are being tested in different models to reduce fibrosis and improve adhesion after surgery, including Telmisartan, valsartan, and enalapril. Conclusion: Identification of the pathological causes of post-surgical adhesion and the potential role of targeting Renin–Angiotensin System may help prevent this problem. Based on the pathological function of RAS signaling after surgeries, the administration of ARBs may be considered as a novel and efficient approach to prevent postsurgical adhesions. Pre-clinical and clinical studies should be carried out to have better information on the clinical significance of this therapy against post-surgical adhesion formation.

scholarly journals Severe Acute Respiratory Syndrome Coronavirus 2, COVID-19, and the Renin-Angiotensin System

Hypertension ◽  
2020 ◽  
Vol 76 (5) ◽  
pp. 1350-1367 ◽  
Author(s):  
Matthew A. Sparks ◽  
Andrew M. South ◽  
Andrew D. Badley ◽  
Carissa M. Baker-Smith ◽  
Daniel Batlle ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Renin Angiotensin System ◽  
Organ Damage ◽  
Experimental Models ◽  
Multiple Organ ◽  
Host Cells ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Organ Systems

The coronavirus disease 2019 (COVID-19) pandemic is associated with significant morbidity and mortality throughout the world, predominantly due to lung and cardiovascular injury. The virus responsible for COVID-19—severe acute respiratory syndrome coronavirus 2—gains entry into host cells via ACE2 (angiotensin-converting enzyme 2). ACE2 is a primary enzyme within the key counter-regulatory pathway of the renin-angiotensin system (RAS), which acts to oppose the actions of Ang (angiotensin) II by generating Ang-(1–7) to reduce inflammation and fibrosis and mitigate end organ damage. As COVID-19 spans multiple organ systems linked to the cardiovascular system, it is imperative to understand clearly how severe acute respiratory syndrome coronavirus 2 may affect the multifaceted RAS. In addition, recognition of the role of ACE2 and the RAS in COVID-19 has renewed interest in its role in the pathophysiology of cardiovascular disease in general. We provide researchers with a framework of best practices in basic and clinical research to interrogate the RAS using appropriate methodology, especially those who are relatively new to the field. This is crucial, as there are many limitations inherent in investigating the RAS in experimental models and in humans. We discuss sound methodological approaches to quantifying enzyme content and activity (ACE, ACE2), peptides (Ang II, Ang-[1–7]), and receptors (types 1 and 2 Ang II receptors, Mas receptor). Our goal is to ensure appropriate research methodology for investigations of the RAS in patients with severe acute respiratory syndrome coronavirus 2 and COVID-19 to ensure optimal rigor and reproducibility and appropriate interpretation of results from these investigations.

scholarly journals Renin-Angiotensin System Blockade Improves Endothelial Dysfunction in Hypertension

Hypertension ◽  
2000 ◽  
Vol 36 (4) ◽  
pp. 575-580 ◽  
Author(s):  
Kenichi Goto ◽  
Koji Fujii ◽  
Uran Onaka ◽  
Isao Abe ◽  
Masatoshi Fujishima
Keyword(s):  
Endothelial Dysfunction ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Quantifying Renin-Angiotensin-System Alterations in COVID-19

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2755
Author(s):  
Fabrizio Pucci ◽  
Filippo Annoni ◽  
Robson Augusto Souza dos Santos ◽  
Fabio Silvio Taccone ◽  
Marianne Rooman
Keyword(s):  
Meta Analysis ◽  
Renin Angiotensin System ◽  
Host Cells ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Physiological Processes ◽  
Open Questions ◽  
Clinical Investigations ◽  
Conflicting Evidence

The renin-angiotensin system (RAS) plays a pivotal role in a wide series of physiological processes, among which inflammation and blood pressure regulation. One of its key components, the angiotensin-converting enzyme 2, has been identified as the entry point of the SARS-CoV-2 virus into the host cells, and therefore a lot of research has been devoted to study RAS dysregulation in COVID-19. Here we discuss the alterations of the regulatory RAS axes due to SARS-CoV-2 infection on the basis of a series of recent clinical investigations and experimental analyzes quantifying, e.g., the levels and activity of RAS components. We performed a comprehensive meta-analysis of these data in view of disentangling the links between the impaired RAS functioning and the pathophysiological characteristics of COVID-19. We also review the effects of several RAS-targeting drugs and how they could potentially help restore the normal RAS functionality and minimize the COVID-19 severity. Finally, we discuss the conflicting evidence found in the literature and the open questions on RAS dysregulation in SARS-CoV-2 infection whose resolution would improve our understanding of COVID-19.

scholarly journals Angiotensin-(1-7): Translational Avenues in Cardiovascular Control

2019 ◽  
Vol 32 (12) ◽  
pp. 1133-1142 ◽  
Author(s):  
Daniela Medina ◽  
Amy C Arnold
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Current Knowledge ◽  
Renin Angiotensin System ◽  
Cardiovascular Control ◽  
Biologically Active ◽  
Global Public Health ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Cardiovascular Actions

Abstract Despite decades of research and numerous treatment approaches, hypertension and cardiovascular disease remain leading global public health problems. A major contributor to regulation of blood pressure, and the development of hypertension, is the renin-angiotensin system. Of particular concern, uncontrolled activation of angiotensin II contributes to hypertension and associated cardiovascular risk, with antihypertensive therapies currently available to block the formation and deleterious actions of this hormone. More recently, angiotensin-(1–7) has emerged as a biologically active intermediate of the vasodilatory arm of the renin-angiotensin system. This hormone antagonizes angiotensin II actions as well as offers antihypertensive, antihypertrophic, antiatherogenic, antiarrhythmogenic, antifibrotic and antithrombotic properties. Angiotensin-(1–7) elicits beneficial cardiovascular actions through mas G protein-coupled receptors, which are found in numerous tissues pivotal to control of blood pressure including the brain, heart, kidneys, and vasculature. Despite accumulating evidence for favorable effects of angiotensin-(1–7) in animal models, there is a paucity of clinical studies and pharmacokinetic limitations, thus limiting the development of therapeutic agents to better understand cardiovascular actions of this vasodilatory peptide hormone in humans. This review highlights current knowledge on the role of angiotensin-(1–7) in cardiovascular control, with an emphasis on significant animal, human, and therapeutic research efforts.

scholarly journals Cadmium exposure activates NADPH oxidase, renin–angiotensin system and cyclooxygenase 2 pathways in arteries, inducing hypertension and vascular damage

2020 ◽  
Vol 333 ◽  
pp. 80-89 ◽  
Author(s):  
José Eudes Gomes Pinheiro Júnior ◽  
Paola Zambelli Moraes ◽  
Marina Diaz Rodriguez ◽  
Maylla Ronacher Simões ◽  
Francielli Cibin ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Renin Angiotensin System ◽  
Cyclooxygenase 2 ◽  
Cadmium Exposure ◽  
Vascular Damage ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals RAS in Pregnancy and Preeclampsia and Eclampsia

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
M. Rodriguez ◽  
J. Moreno ◽  
J. Hasbun
Keyword(s):  
Endothelial Dysfunction ◽  
Renin Angiotensin System ◽  
Common Disease ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Multisystem Involvement ◽  
The Brain ◽  
In Pregnancy

Preeclampsia is a common disease of pregnancy characterized by the presence of hypertension and commitment of many organs, including the brain, secondary to generalized endothelial dysfunction. Its etiology is not known precisely, but it involved several factors, highlighting the renin angiotensin system (RAS), which would have an important role in the origin of multisystem involvement. This paper reviews the evidence supporting the involvement of RAS in triggering the disease, in addition to the components of this system that would be involved and how it eventually produces brain engagement.

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