Increased complications of COVID-19 in people with cardiovascular disease: Role of the renin-angiotensin-aldosterone system (RAAS) dysregulation.

Augustine, R; S, A; Nayeem, A; Salam, SA; Augustine, P; Dan, P; Monteiro, P; Mraiche, F; Gentile, C; Hansbro, PM; McClements, L; Hasan, A

Increased complications of COVID-19 in people with cardiovascular disease: Role of the renin-angiotensin-aldosterone system (RAAS) dysregulation.

Augustine, R S, A Nayeem, A Salam, SA Augustine, P Dan, P Monteiro, P Mraiche, F Gentile, C

Hansbro, PM McClements, L

Hasan, A

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Publisher:: Elsevier BV
Publication Type:: Journal Article
Citation:: Chemico-biological interactions, 2021, 351, pp. 109738
Issue Date:: 2021-11-02

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Field	Value	Language
dc.contributor.author	Augustine, R
dc.contributor.author	S, A
dc.contributor.author	Nayeem, A
dc.contributor.author	Salam, SA
dc.contributor.author	Augustine, P
dc.contributor.author	Dan, P
dc.contributor.author	Monteiro, P
dc.contributor.author	Mraiche, F
dc.contributor.author	Gentile, C https://orcid.org/0000-0002-3689-4275
dc.contributor.author	Hansbro, PM
dc.contributor.author	McClements, L https://orcid.org/0000-0002-4911-1014
dc.contributor.author	Hasan, A
dc.date.accessioned	2021-11-29T10:55:34Z
dc.date.available	2021-11-01
dc.date.available	2021-11-29T10:55:34Z
dc.date.issued	2021-11-02
dc.identifier.citation	Chemico-biological interactions, 2021, 351, pp. 109738
dc.identifier.issn	0009-2797
dc.identifier.issn	1872-7786
dc.identifier.uri	http://hdl.handle.net/10453/151908
dc.description.abstract	The rapid spread of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19), has had a dramatic negative impact on public health and economies worldwide. Recent studies on COVID-19 complications and mortality rates suggest that there is a higher prevalence in cardiovascular diseases (CVD) patients. Past investigations on the associations between pre-existing CVDs and susceptibility to coronavirus infections including SARS-CoV and the Middle East Respiratory Syndrome coronavirus (MERS-CoV), have demonstrated similar results. However, the underlying mechanisms are poorly understood. This has impeded adequate risk stratification and treatment strategies for CVD patients with SARS-CoV-2 infections. Generally, dysregulation of the expression of angiotensin-converting enzyme (ACE) and the counter regulator, angiotensin-converting enzyme 2 (ACE2) is a hallmark of cardiovascular risk and CVD. ACE2 is the main host receptor for SARS-CoV-2. Although further studies are required, dysfunction of ACE2 after virus binding and dysregulation of the renin-angiotensin-aldosterone system (RAAS) signaling may worsen the outcomes of people affected by COVID-19 and with preexisting CVD. Here, we review the current knowledge and outline the gaps related to the relationship between CVD and COVID-19 with a focus on the RAAS. Improved understanding of the mechanisms regulating viral entry and the role RAAS may direct future research with the potential to improve the prevention and management of COVID-19.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	Elsevier BV
dc.relation	http://purl.org/au-research/grants/nhmrc/1175134
dc.relation	Catholic Archdiocese of Sydney
dc.relation.ispartof	Chemico-biological interactions
dc.relation.isbasedon	10.1016/j.cbi.2021.109738
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	0601 Biochemistry and Cell Biology
dc.subject.classification	Toxicology
dc.title	Increased complications of COVID-19 in people with cardiovascular disease: Role of the renin-angiotensin-aldosterone system (RAAS) dysregulation.
dc.type	Journal Article
utslib.citation.volume	351
utslib.location.activity	Ireland
utslib.for	0601 Biochemistry and Cell Biology
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
pubs.organisational-group	/University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering
pubs.organisational-group	/University of Technology Sydney/Strength - IBMD - Initiative for Biomedical Devices
pubs.organisational-group	/University of Technology Sydney/Centre for Health Technologies (CHT)
utslib.copyright.status	open_access	*
dc.date.updated	2021-11-29T10:55:26Z
pubs.publication-status	Published
pubs.volume	351

Abstract:

The rapid spread of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) that causes coronavirus disease 2019 (COVID-19), has had a dramatic negative impact on public health and economies worldwide. Recent studies on COVID-19 complications and mortality rates suggest that there is a higher prevalence in cardiovascular diseases (CVD) patients. Past investigations on the associations between pre-existing CVDs and susceptibility to coronavirus infections including SARS-CoV and the Middle East Respiratory Syndrome coronavirus (MERS-CoV), have demonstrated similar results. However, the underlying mechanisms are poorly understood. This has impeded adequate risk stratification and treatment strategies for CVD patients with SARS-CoV-2 infections. Generally, dysregulation of the expression of angiotensin-converting enzyme (ACE) and the counter regulator, angiotensin-converting enzyme 2 (ACE2) is a hallmark of cardiovascular risk and CVD. ACE2 is the main host receptor for SARS-CoV-2. Although further studies are required, dysfunction of ACE2 after virus binding and dysregulation of the renin-angiotensin-aldosterone system (RAAS) signaling may worsen the outcomes of people affected by COVID-19 and with preexisting CVD. Here, we review the current knowledge and outline the gaps related to the relationship between CVD and COVID-19 with a focus on the RAAS. Improved understanding of the mechanisms regulating viral entry and the role RAAS may direct future research with the potential to improve the prevention and management of COVID-19.

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http://hdl.handle.net/10453/151908