Response by Gheblawi et al to Letter Regarding Article, “Angiotensin-Converting Enzyme 2: SARS-CoV-2 Receptor and Regulator of the Renin-Angiotensin System: Celebrating the 20th Anniversary of the Discovery of ACE2”

Gheblawi, Mahmoud; Wang, Kaiming; Viveiros, Anissa; Nguyen, Quynh; Zhong, Jiuchang; Turner, Anthony J.; Raizada, Mohan K.; Grant, Maria B.; Oudit, Gavin Y.

doi:10.1161/circresaha.120.317332

Cited by 270 publications

(470 citation statements)

References 9 publications

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“…ACE2 is a monocarboxypeptidase that mitigates the deleterious actions of Ang II by converting it into the heptapeptide Ang-(1-7) [60,61]. ACE2 has been identified as the functional receptor for SARS-CoV-1 [62] as well as the SARS-CoV-2 receptor [63][64][65].…”

Section: Ace2: Linking the Renin-angiotensin System Obesity-relatedmentioning

confidence: 99%

“…The interaction between the SARS viruses and ACE2 has been proposed as a potential factor in their infectivity [67,68]. Like other RAAS components, ACE2 is expressed in many tissues, including the lungs, cardiovascular system, gut, kidneys, pancreas, testis, central nervous system, and adipose tissue [60]. It has been suggested that alveolar macrophages expressing ACE2 are the primary target cells for SARS-CoV-2 infection, and these activated macrophages may play a major role in the cytokine storm during COVID-19 [69].…”

Section: Ace2: Linking the Renin-angiotensin System Obesity-relatedmentioning

confidence: 99%

See 1 more Smart Citation

Obesity and COVID-19: A Perspective from the European Association for the Study of Obesity on Immunological Perturbations, Therapeutic Challenges, and Opportunities in Obesity

et al. 2020

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Accumulating evidence suggests that obesity is a major risk factor for the initiation, progression, and outcomes of coronavirus disease 2019 (COVID-19). The European Association for the Study of Obesity (EASO), as a scientific and medical society dedicated to the promotion of health and well-being, is greatly concerned about the concomitant obesity and COVID-19 pandemics and their impact on health and society at large. In this perspective, we will address the inherent immunological perturbations and alterations in the renin-angiotensin-aldosterone system in patients with obesity and COVID-19, and discuss how these impairments may underlie the increased susceptibility and more detrimental outcomes of COVID-19 in people with obesity. Clearly, this has important implications for preventive measures, vaccination, and future therapeutic strategies to combat COVID-19. Furthermore, we will highlight important knowledge gaps and provide suggestions for future research and recommendations for policy actions. Since many new reports on COVID-19 rapidly appear, the present perspective should be seen as a focus for discussion to drive forward further understanding, research initiatives, and clinical management of COVID-19.

show abstract

Section: Ace2: Linking the Renin-angiotensin System Obesity-relatedmentioning

confidence: 99%

Section: Ace2: Linking the Renin-angiotensin System Obesity-relatedmentioning

confidence: 99%

Obesity and COVID-19: A Perspective from the European Association for the Study of Obesity on Immunological Perturbations, Therapeutic Challenges, and Opportunities in Obesity

et al. 2020

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“…Cardiogenic shock due to myocarditis has been extensively reported as among the most common cardiovascular complications of COVID-19 [ 3 ]. Previous studies have reported that angiotensin-converting enzyme 2 (ACE2) receptors mediated effects on lungs, kidneys, heart, vascular endothelium by downregulating their expression and enhanced vasoconstriction with deleterious effects of the unopposed reticuloendothelial system [ 4 ]. It is also likely that virus-mediated immune response can cause consumption coagulopathies, acute hemolytic anemias, and other blood cell dyscrasias [ 3 , 5 - 6 ].…”

Section: Discussionmentioning

confidence: 99%

A Case of Hemolytic Anemia With Acute Myocarditis and Cardiogenic Shock: A Rare Presentation of COVID-19

Singhavi¹,

Sharma²,

Desai³

et al. 2020

Cureus

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Coronavirus disease 2019 (COVID-19) cases are on the rise globally, and mortality- and survival-related data are emerging every day. In addition, upcoming reports are suggestive of increased risk of cardiac ailments in high-risk patients. In the context of cardiac involvement, acute myocarditis has become one of the unexplored areas in COVID-19 patients, which could influence the long-term outcomes. In this report, we present a rare case that warrants further study on the subject due to the paucity of data in the literature. To date, no case of severe hemolytic anemias with stress cardiomyopathy/acute myocarditis in a patient of COVID-19 has been formally reported in the literature. The bedside echocardiogram had shown a possibility of acute myocarditis. The patient’s marked left ventricular (LV) functional recovery without coronary intervention further corroborates the same. Clinicians should be aware of the diversity of cardiovascular/hematological complications, as well as focused cardiac ultrasound study and the importance of echocardiography as a good screening modality for cardiovascular and hematological complications of COVID-19 infection.

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“…1 SARS-CoV-1 downregulates ACE2, with a subsequent increase in angiotensin II (ANGII) levels, 2 which potentially creates a dysregulation with overactivation of the Renin-Angiotensin-Aldosterone System (RAAS). 3 The RAAS is a hormonal system contributing to the control of circulating blood volume, blood pressure and is often pharmaceutically manipulated in hypertonic disease. 4 Current clinical management guidelines for the coronavirus disease 2019 (COVID- 19) are mainly centered around the assumption that SARS-CoV-2 directly results in an acute lung parenchymal disease.…”

Section: Introductionmentioning

confidence: 99%

COVID-19 pathophysiology may be driven by a loss of inhibition of the Renin-Angiotensin-Aldosterone System

Rysz¹,

Al-Saadi²,

Sjöström³

et al. 2020

Preprint

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SARS-CoV-2 enters the cell through the ACE2 receptor, which is considered one of the main inhibitors in the Renin-Angiotensin-Aldosterone System (RAAS).1 ,2 The virus has been shown to downregulate the ACE2 receptor, leading to a subsequent increase in the vasopressoragentangiotensinII.3 Evidently,criticalcoronavirusdisease2019(COVID-19)is thought to be due to a dysregulated immune response, causing a cytokine-release syndrome eventually leading to acute respiratory distress syndrome (ARDS).4 ,5 However, several reports on clinical laboratory features and case-descriptions of critically ill patients with COVID-19 show discrepancies compared to typical ARDS. Here, we show that infusing swines with angiotensin II induces a pathophysiological syndrome closely resembling that of patients with RT-PCR-positive COVID-19. By using multimodal clinical imaging of patients, comparing laboratory data and translational histological features, we show that it is highly likely that an increase in RAAS is one, if not the main, pathogenic feature in critical COVID-19. Furthermore, it is plausible that this large animal model can be used to screen for potential new treatments for patients with severe COVID-19 and that MRI lung perfusion can be used to evaluate the outcome of potential treatments targeting the pathophysiological syndrome.

show abstract

Response by Gheblawi et al to Letter Regarding Article, “Angiotensin-Converting Enzyme 2: SARS-CoV-2 Receptor and Regulator of the Renin-Angiotensin System: Celebrating the 20th Anniversary of the Discovery of ACE2”

Cited by 270 publications

References 9 publications

Obesity and COVID-19: A Perspective from the European Association for the Study of Obesity on Immunological Perturbations, Therapeutic Challenges, and Opportunities in Obesity

Obesity and COVID-19: A Perspective from the European Association for the Study of Obesity on Immunological Perturbations, Therapeutic Challenges, and Opportunities in Obesity

A Case of Hemolytic Anemia With Acute Myocarditis and Cardiogenic Shock: A Rare Presentation of COVID-19

COVID-19 pathophysiology may be driven by a loss of inhibition of the Renin-Angiotensin-Aldosterone System

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