Genetic Polymorphism of Angiotensin II Type 1 Receptors and Their Effect on the Clinical Outcome of Captopril Treatment in Arab Iraqi Patients with Acute Coronary Syndrome (Mid Euphrates)

Ghafil, Fadhaa Abdulameer; Mohammad, Bassim I; Al-Janabi, Hussain S.; Hadi, Najah R.; Al-Aubaidy, Hayder A.

doi:10.1007/s12291-019-00860-x

Cited by 5 publications

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References 26 publications

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“…The RAS is a metabolic cascade involved in the regulation of cardiovascular homoeostasis and cardiac remodeling [27]. Besides regulating blood pressure and circulating blood volume as well as fluid and salt balance [28,29], this system also has a significant role in atherosclerosis pathogenesis and in endothelial dysfunction [17,30]. RAS major components are renin, angiotensin, AGT, ACE and AT1R [31].…”

Section: Ras and Covid-19 21 Ras: A Portal Entry For Sars-cov-2mentioning

confidence: 99%

The Renin-Angiotensin System: A Key Role in SARS-CoV-2-Induced COVID-19

et al. 2021

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The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), was first identified in Eastern Asia (Wuhan, China) in December 2019. The virus then spread to Europe and across all continents where it has led to higher mortality and morbidity, and was declared as a pandemic by the World Health Organization (WHO) in March 2020. Recently, different vaccines have been produced and seem to be more or less effective in protecting from COVID-19. The renin–angiotensin system (RAS), an essential enzymatic cascade involved in maintaining blood pressure and electrolyte balance, is involved in the pathogenicity of COVID-19, since the angiotensin-converting enzyme II (ACE2) acts as the cellular receptor for SARS-CoV-2 in many human tissues and organs. In fact, the viral entrance promotes a downregulation of ACE2 followed by RAS balance dysregulation and an overactivation of the angiotensin II (Ang II)–angiotensin II type I receptor (AT1R) axis, which is characterized by a strong vasoconstriction and the induction of the profibrotic, proapoptotic and proinflammatory signalizations in the lungs and other organs. This mechanism features a massive cytokine storm, hypercoagulation, an acute respiratory distress syndrome (ARDS) and subsequent multiple organ damage. While all individuals are vulnerable to SARS-CoV-2, the disease outcome and severity differ among people and countries and depend on a dual interaction between the virus and the affected host. Many studies have already pointed out the importance of host genetic polymorphisms (especially in the RAS) as well as other related factors such age, gender, lifestyle and habits and underlying pathologies or comorbidities (diabetes and cardiovascular diseases) that could render individuals at higher risk of infection and pathogenicity. In this review, we explore the correlation between all these risk factors as well as how and why they could account for severe post-COVID-19 complications.

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