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Genes encoding ACE2, TMPRSS2 and related proteins mediating SARS-CoV-2 viral entry are upregulated with age in human cardiomyocytes.

Accepted version
Peer-reviewed

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Type

Article

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Authors

Robinson, Emma L 
Alkass, Kanar 
Bergmann, Olaf 
Maguire, Janet J 
Roderick, H Llewelyn 

Abstract

Age (>70 years), case fatality rate (CFR,10.2%) and coexisting conditions, particularly cardiovascular disease (CFR,10.5%) and hypertension (CFR,6.0%), are independent predictors of adverse outcome for 45,000 COVID-19 patients in China [1]. A consensus has emerged that SARS-CoV-2 uses the same ‘receptor’ as SARS-CoV, the angiotensin converting enzyme 2 (ACE2), for initial binding to the host cell. This must be co-expressed with the serine protease TMPRSS2, that primes the spike protein S1 for endocytosis-mediated internalization of virus, employing the S2 domain for fusion to the host membrane (Figure [1A])[2-4]. A key difference in SARS-CoV-2 is a spike protein second site (S2’), proposed to be cleaved by the proteinase furin2. Once inside the cell cysteine proteases, cathepsin L and B, are thought critical for endosomal processing in certain cells [3-4].

Description

Keywords

Angiotensin, Apelin, Bradykinin, COVID-19, Human cardiomyocytes, RNA-sequencing, SARS-CoV-2, Aging, Angiotensin-Converting Enzyme 2, Angiotensins, Apelin, Betacoronavirus, Bradykinin, COVID-19, Cathepsin B, Cathepsin L, Coronavirus Infections, Humans, Myocardium, Myocytes, Cardiac, Pandemics, Peptidyl-Dipeptidase A, Pneumonia, Viral, SARS-CoV-2, Serine Endopeptidases, Virus Attachment, Virus Internalization

Journal Title

J Mol Cell Cardiol

Conference Name

Journal ISSN

0022-2828
1095-8584

Volume Title

147

Publisher

Elsevier BV
Sponsorship
Wellcome Trust (107715/Z/15/Z)
British Heart Foundation (TG/18/4/33770)
MRC (MC_PC_14116 v2)
Wellcome Trust (090663/Z/09/A)
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