scholarly journals Loss of Angiotensin-Converting Enzyme-2 Exacerbates Diabetic Cardiovascular Complications and Leads to Systolic and Vascular Dysfunction

2012 ◽  
Vol 110 (10) ◽  
pp. 1322-1335 ◽  
Author(s):  
Vaibhav B. Patel ◽  
Sreedhar Bodiga ◽  
Ratnadeep Basu ◽  
Subhash K. Das ◽  
Wang Wang ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Vascular Dysfunction ◽  
Cardiovascular Complications ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2

scholarly journals The regulation of ACE-2 in the heart and lungs

2021 ◽  
Vol 9 (40) ◽  
pp. 47-52
Author(s):  
Jonathan Kopel ◽  
Thomas Tenner ◽  
Gregory Brower
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Cardiovascular Disease ◽  
Angiotensin Converting Enzyme ◽  
Molecular Mechanisms ◽  
Physiological Responses ◽  
Cardiovascular Complications ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Metabolism Regulation

The pathogenesis of SARS-CoV-2 infection or COVID-19 disease remains an active and rapidly evolving area of investigation. Currently, the angiotensin-converting enzyme 2 protein (ACE-2) is the primary receptor implicated in the pathogenesis of SARS-CoV-2. In normal physiological responses, the ACE-2 has important roles in regulating the renin-angiotensin systems (RAS) in several organs, including the heart, kidney, and lungs. Dysregulation of ACE-2 has been linked to heart failure, pulmonary hypertension, and diabetic cardiovascular complications. Two main risk factors for COVID-19 include hypertension and cardiovascular disease. However, the precise mechanism causing these risk factors for COVID-19 infectivity remains unknown. In this paper, we provide possible molecular mechanisms that underlie the cardiovascular risk factors for COVID-19. Keywords: SARS-CoV-2, COVID-19, angiotensin converting enzyme-2 (ACE-2), hormones, cardiovascular, hypoxia, metabolism, regulation, and pathophysiology

scholarly journals Dampak Coronavirus Disease 2019 terhadap Sistem Kardiovaskular

e-CliniC ◽  
2020 ◽  
Vol 8 (2) ◽  
Author(s):  
Herick A. Willim ◽  
Infan Ketaren ◽  
Alice I. Supit
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Angiotensin Converting Enzyme ◽  
Myocardial Injury ◽  
Clinical Manifestations ◽  
Cardiovascular Complications ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Cardiovascular Comorbidity ◽  
Cardiovascular Comorbidities ◽  
Severe Manifestation

Abstract: Coronavirus disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection has become a pandemic. Patient with cardiovascular comorbidity has a higher risk of suffering more severe manifestation of COVID-19 associated with a higher mortality. Although dominated by respiratory clinical manifestation, COVID-19 may also cause severe cardiovascular disorders. Angiotensin converting enzyme 2 (ACE2) acts as a receptor of SARS-CoV-2. Patients of COVID-19 with cardiovascular comorbidities may experience more severe clinical manifestations, presumably due to higher ACE2 expression in this population. Cardiovascular complications in COVID-19 may include myocardial injury, myocarditis, acute myocardial infarction, acute heart failure, thromboembolism, and arrhythmias. Therefore, optimization of conservative medical therapy needs to be prioritized in patients with cardiovascular comorbidities. Emergency intervention can be considered in certain cases with hemodynamic instability.Keywords: cardiovascular system, COVID-19, SARS-CoV-2, ACE2 Abstrak: Coronavirus disease 2019 (COVID-19) telah merupakan pandemi yang disebabkan oleh infeksi Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). Pasien dengan komorbid kardiovaskular berisiko lebih tinggi untuk mengalami manifestasi yang lebih berat jika terinfeksi COVID-19 dan berhubungan dengan mortalitas yang lebih tinggi. Meskipun didominasi oleh manifestasi klinis respiratorik, COVID-19 juga dapat menyebabkan gangguan kardiovaskular yang berat. Angiotensin converting enzyme 2 (ACE2) berperan sebagai reseptor SARS-CoV-2. Diduga pasien dengan penyakit kardiovaskular dapat bermanifestasi klinis lebih berat karena ekspresi ACE2 yang lebih tinggi pada populasi ini. Komplikasi kardiovaskular pada COVID-19 dapat meliputi jejas miokardium, miokarditis, infark miokard akut, gagal jantung akut, tromboemboli, dan aritmia. Pada pasien dengan komorbid kardiovaskular, optimalisasi terapi medis konservatif perlu diprioritaskan. Tindakan intervensi darurat dapat dipertimbangkan pada kasus tertentu dengan instabilitas hemodinamik.Kata kunci: sistem kardiovaskular, COVID-19, SARS-CoV-2, ACE2

Thermodynamics of the interaction between the spike protein of severe acute respiratory syndrome- coronavirus-2 and the receptor of human angiotensin converting enzyme 2. Effects of possible ligands

2020 ◽  
Author(s):  
Cristina Garcia-Iriepa ◽  
Cecilia Hognon ◽  
Antonio Francés-Monerris ◽  
Isabel Iriepa ◽  
Tom Miclot ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Molecular Mechanisms ◽  
Molecular Design ◽  
Binding Free Energy ◽  
Transmembrane Protein ◽  
Spike Protein ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Rational Molecular Design ◽  
Rational Evaluation

<div><p>Since the end of 2019, the coronavirus SARS-CoV-2 has caused more than 180,000 deaths all over the world, still lacking a medical treatment despite the concerns of the whole scientific community. Human Angiotensin-Converting Enzyme 2 (ACE2) was recently recognized as the transmembrane protein serving as SARS-CoV-2 entry point into cells, thus constituting the first biomolecular event leading to COVID-19 disease. Here, by means of a state-of-the-art computational approach, we propose a rational evaluation of the molecular mechanisms behind the formation of the complex and of the effects of possible ligands. Moreover, binding free energy between ACE2 and the active Receptor Binding Domain (RBD) of the SARS-CoV-2 spike protein is evaluated quantitatively, assessing the molecular mechanisms at the basis of the recognition and the ligand-induced decreased affinity. These results boost the knowledge on the molecular grounds of the SARS-CoV-2 infection and allow to suggest rationales useful for the subsequent rational molecular design to treat severe COVID-19 cases.</p></div>

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