About: Hypertension and renin-angiotensin system blockers are not associated with expression of Angiotensin Converting Enzyme 2 (ACE2) in the kidney

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About: Hypertension and renin-angiotensin system blockers are not associated with expression of Angiotensin Converting Enzyme 2 (ACE2) in the kidney Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Hypertension and renin-angiotensin system blockers are not associated with expression of Angiotensin Converting Enzyme 2 (ACE2) in the kidney
Creator	Morris, Andrew Jiang, Xiao Burrell, Louise Williams, Bryan Guzik, Tomasz Charchar, Fadi Eales, James Tomaszewski, Maciej Xu, Xiaoguang Antczak, Andrzej Bogdanski, Pawel Byars, Sean Cano-Gamez, Eddie Denniff, Matthew Glyda, Maciej Greenstein, Adam Harrap, Stephen Heagerty, Anthony Keavney, Bernard Król, Robert Maier, Michelle Nazgiewicz, Alicja Prestes, Priscilla Saluja, Sushant Samani, Nilesh Scannali, David Szulinska, Monika Trynka, Gosia Woolf, Adrian Wystrychowski, Wojciech Zukowska-Szczechowska, Ewa Zywiec, Joanna
Source	MedRxiv
abstract	Angiotensin converting enzyme 2 (ACE2) is the cellular entry point for severe acute respiratory syndrome coronavirus (SARS-CoV-2) - the cause of COVID-19 disease. It has been hypothesized that use of renin-angiotensin system (RAS) inhibiting medications in patients with hypertension, increases the expression of ACE2 and thereby increases the risk of COVID-19 infection and severe outcomes or death. However, the effect of RAS-inhibition on ACE2 expression in human tissues of key relevance to blood pressure regulation and COVID-19 infection has not previously been reported. We examined how hypertension, its major metabolic co-phenotypes and antihypertensive medications relate to ACE2 renal expression using information from up to 436 patients whose kidney transcriptomes were characterised by RNA-sequencing. We further validated some of the key observations in other human tissues and/or a controlled experimental model. Our data reveal increasing expression of ACE2 with age in both human lungs and the kidney. We show no association between renal expression of ACE2 and either hypertension or common types of RAS inhibiting drugs. We demonstrate that renal abundance of ACE2 is positively associated with a biochemical index of kidney function and show a strong enrichment for genes responsible for kidney health and disease in ACE2 co-expression analysis. Collectively, our data indicate that neither hypertension nor antihypertensive treatment are likely to alter individual risk of SARS-CoV-2 infection or influence clinical outcomes in COVID-19 through changes of ACE2 expression. Our data further suggest that in the absence of SARS-CoV-2 infection, kidney ACE2 is most likely nephro-protective but the age-related increase in its expression within lungs and kidneys may be relevant to the risk of SARS-CoV-2 infection.
has issue date	2020-05-26(xsd:dateTime)
bibo:doi	10.1101/2020.05.19.20106781
has license	medrxiv
sha1sum (hex)	82ebea8b9ba6d836a28f89c058427d0eb44c33c0
schema:url	https://doi.org/10.1101/2020.05.19.20106781
resource representing a document's title	Hypertension and renin-angiotensin system blockers are not associated with expression of Angiotensin Converting Enzyme 2 (ACE2) in the kidney
resource representing a document's body	covid:82ebea8b9ba6d836a28f89c058427d0eb44c33c0#body_text
is schema:about of	named entity 'ACE2' named entity 'expression' named entity 'metabolic' named entity 'hypertension' named entity 'entry point' named entity 'EFFECT' named entity 'DISEASE' named entity 'LUNGS' named entity 'kidneys' named entity 'medications' named entity 'COVID-19' named entity 'ACE2' named entity 'hypothesized' named entity 'However' named entity 'Our' named entity 'Angiotensin' named entity 'ACE2' named entity 'phenotypes' named entity 'antihypertensive treatment' named entity 'transcriptomes' named entity 'COVID-19 infection' named entity 'ACE2' named entity 'ACE2' named entity 'ACE2' named entity 'SARS-CoV-2' named entity 'RAS' named entity 'biochemical' named entity 'severe acute respiratory syndrome coronavirus' named entity 'blood pressure regulation' named entity 'kidney' named entity 'ACE2' named entity 'hypertension' named entity 'metabolic' named entity 'kidney' named entity 'RNA-sequencing' named entity 'SARS-CoV-2' named entity 'USP9Y' named entity 'expression analysis' named entity 'infection' named entity 'diabetes' named entity 'P-values' named entity 'RAS' named entity 'kidney' named entity 'NIH' named entity 'dependent variable' named entity 'post-transcriptional' named entity 'human organs' named entity 'kidneys' named entity 'diabetes' named entity 'perindopril' named entity 'antihypertensive' named entity 'heterozygosity' named entity 'gene expression' named entity 'cell type'

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