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SARS-CoV-2 and the cardiovascular system.

ABSTRACT: The coronavirus disease COVID-19 is a public health emergency caused by a novel coronavirus named severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). SARS-CoV-2 infection uses the angiotensin-converting enzyme 2 (ACE2) receptor, and typically spreads through the respiratory tract. Invading viruses can elicit an exaggerated host immune response, frequently leading to a cytokine storm that may be fueling some COVID-19 death. This response contributes to multi-organ dysfunction. Accumulating data points to an increased cardiovascular disease morbidity, and mortality in COVID-19 patients. This brief review explores potential available evidence regarding the association between COVID-19, and cardiovascular complications.

SUBMITTER: Hafiane A

PROVIDER: S-EPMC7363601 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

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SARS-CoV-2 and the cardiovascular system.

Hafiane Anouar A

Clinica chimica acta; international journal of clinical chemistry 20200716

The coronavirus disease COVID-19 is a public health emergency caused by a novel coronavirus named severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). SARS-CoV-2 infection uses the angiotensin-converting enzyme 2 (ACE2) receptor, and typically spreads through the respiratory tract. Invading viruses can elicit an exaggerated host immune response, frequently leading to a cytokine storm that may be fueling some COVID-19 death. This response contributes to multi-organ dysfunction. Accumulat ...[more]

PMID: 32681935

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Project description:The current COVID-19 pandemic started several months ago and is still exponentially growing in most parts of the world - this is the most recent and alarming update. COVID-19 requires the collaboration of nearly 200 countries to curb the spread of SARS-CoV-2 while gaining time to explore and improve treatment options especially for cardiovascular disease (CVD) and immunocompromised patients, who appear to be at high-risk to die from cardiopulmonary failure. Currently unanswered questions are why elderly people, particularly those with pre-existing comorbidities seem to exhibit higher mortality rates after SARS-CoV-2 infection and whether intensive care becomes indispensable for these patients to prevent multi-organ failure and sudden death. To face these challenges, we here summarize the molecular insights into viral infection mechanisms and implications for cardiovascular disease. Since the infection starts in the upper respiratory system, first flu-like symptoms develop that spread throughout the body. The wide range of affected organs is presumably based on the common expression of the major SARS-CoV-2 entry-receptor angiotensin-converting enzyme 2 (ACE2). Physiologically, ACE2 degrades angiotensin II, the master regulator of the renin-angiotensin-aldosterone system (RAAS), thereby converting it into vasodilatory molecules, which have well-documented cardio-protective effects. Thus, RAAS inhibitors, which may increase the expression levels of ACE2, are commonly used for the treatment of hypertension and CVD. This, and the fact that SARS-CoV-2 hijacks ACE2 for cell-entry, have spurred controversial discussions on the role of ACE2 in COVID-19 patients. In this review, we highlight the state-of-the-art knowledge on SARS-CoV-2-dependent mechanisms and the potential interaction with ACE2 expression and cell surface localization. We aim to provide a list of potential treatment options and a better understanding of why CVD is a high risk factor for COVID-19 susceptibility and further discuss the acute as well as long-term cardiac consequences.

Dataset Information

SARS-CoV-2 and the cardiovascular system.

Publications

SARS-CoV-2 and the cardiovascular system.

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