Imperial College London
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DrJamesPeters

Faculty of Medicine, Department of Immunology and Inflammation

Clinical Reader in Rheumatology
 
 
 
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j.peters

 
 
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ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Gill:2020:10.1098/rsos.200958,
author = {Gill, D and Arvanitis, M and Carter, P and Cordero, AIH and Jo, B and Karhunen, V and Larsson, SC and Li, X and Lockhart, SM and Mason, A and Pashos, E and Saha, A and Tan, VY and Zuber, V and Bosse, Y and Fahle, S and Hao, K and Jiang, T and Joubert, P and Lunt, AC and Ouwehand, WH and Roberts, DJ and Timens, W and van, den Berge M and Watkins, NA and Battle, A and Butterworth, AS and Danesh, J and Di, Angelantonio E and Engelhardt, BE and Peters, JE and Sin, DD and Burgess, S},
doi = {10.1098/rsos.200958},
journal = {Royal Society Open Science},
pages = {1--12},
title = {ACE inhibition and cardiometabolic risk factors, lung ACE2 and TMPRSS2 gene expression, and plasma ACE2 levels: a Mendelian randomization study},
url = {http://dx.doi.org/10.1098/rsos.200958},
volume = {7},
year = {2020}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Angiotensin-converting enzyme 2 (ACE2) and serine protease TMPRSS2 have been implicated in cell entry for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease 2019 (COVID-19). The expression of ACE2 and TMPRSS2 in the lung epithelium might have implications for the risk of SARS-CoV-2 infection and severity of COVID-19. We use human genetic variants that proxy angiotensin-converting enzyme (ACE) inhibitor drug effects and cardiovascular risk factors to investigate whether these exposures affect lung ACE2 and TMPRSS2 gene expression and circulating ACE2 levels. We observed no consistent evidence of an association of genetically predicted serum ACE levels with any of our outcomes. There was weak evidence for an association of genetically predicted serum ACE levels with ACE2 gene expression in the Lung eQTL Consortium (p = 0.014), but this finding did not replicate. There was evidence of a positive association of genetic liability to type 2 diabetes mellitus with lung ACE2 gene expression in the Gene-Tissue Expression (GTEx) study (p = 4 × 10−4) and with circulating plasma ACE2 levels in the INTERVAL study (p = 0.03), but not with lung ACE2 expression in the Lung eQTL Consortium study (p = 0.68). There were no associations of genetically proxied liability to the other cardiometabolic traits with any outcome. This study does not provide consistent evidence to support an effect of serum ACE levels (as a proxy for ACE inhibitors) or cardiometabolic risk factors on lung ACE2 and TMPRSS2 expression or plasma ACE2 levels.
AU  - Gill,D
AU  - Arvanitis,M
AU  - Carter,P
AU  - Cordero,AIH
AU  - Jo,B
AU  - Karhunen,V
AU  - Larsson,SC
AU  - Li,X
AU  - Lockhart,SM
AU  - Mason,A
AU  - Pashos,E
AU  - Saha,A
AU  - Tan,VY
AU  - Zuber,V
AU  - Bosse,Y
AU  - Fahle,S
AU  - Hao,K
AU  - Jiang,T
AU  - Joubert,P
AU  - Lunt,AC
AU  - Ouwehand,WH
AU  - Roberts,DJ
AU  - Timens,W
AU  - van,den Berge M
AU  - Watkins,NA
AU  - Battle,A
AU  - Butterworth,AS
AU  - Danesh,J
AU  - Di,Angelantonio E
AU  - Engelhardt,BE
AU  - Peters,JE
AU  - Sin,DD
AU  - Burgess,S
DO  - 10.1098/rsos.200958
EP  - 12
PY  - 2020///
SN  - 2054-5703
SP  - 1
TI  - ACE inhibition and cardiometabolic risk factors, lung ACE2 and TMPRSS2 gene expression, and plasma ACE2 levels: a Mendelian randomization study
T2  - Royal Society Open Science
UR  - http://dx.doi.org/10.1098/rsos.200958
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000595466300001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://royalsocietypublishing.org/doi/10.1098/rsos.200958
UR  - http://hdl.handle.net/10044/1/85352
VL  - 7
ER  -
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