Mediators of SARS-CoV-2 entry are preferentially enriched in cardiomyocytes
Open accessAbstract
Background: The coronavirus disease 2019 (COVID-19) has spread rapidly around the world. In addition to common respiratory symptoms such as cough and fever, some patients also have cardiac injury, however, the mechanism of cardiac injury is not clear. In this study, we analyzed the RNA expression atlases of angiotensin-converting enzyme 2(ACE2), cathepsin B (CTSB) and cathepsin L (CTSL) in the human embryonic heart at single-cell resolution. Results: The results showed that ACE2 was preferentially enriched in cardiomyocytes. Interestingly, serine protease transmembrane serine protease 2 (TMPRSS2) had less expression in cardiomyocytes, but CTSB and CTSL, which belonged to cell protease, could be found to be enriched in cardiomyocytes. The results of enrichment analysis showed that differentially expressed genes (DEGs) in ACE2-positive cardiomyocytes were mainly enriched in the processes of cardiac muscle contraction, regulation of cardiac conduction, mitochondrial respiratory chain, ion channel binding, adrenergic signaling in cardiomyocytes and viral transcription. Conclusions: Our study suggests that both atrial and ventricular cardiomyocytes are potentially susceptible to severe acute respiratory syndrome coronavirus-2(SARS-CoV-2), and SARS-CoV-2 may enter ventricular cardiomyocytes using CTSB/CTSL for S protein priming. This may be the partial cellular mechanism of cardiac injury in patients with COVID-19.
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Cardiomyocytes and pericytes express ACE2 and TMPRSS2, as well as other accessory proteins needed for viral infection by SARS-CoV-2.
“Thus, cardiomyocytes and pericytes express ACE2 and TMPRSS2, as well as other accessory proteins (ie, NRP1 [neuropilin-1 receptor], CD147 , integrin α 5 β 1, and cathepsin B/L) needed for viral infection by SARS-CoV-2”
From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [25]
The cell-type expression atlas reports ACE2 and cathepsin B/L RNA expression in cardiomyocytes, but little TMPRSS2 expression and no ACE2+/TMPRSS2+ cell cluster. The Discussion says the study analyzed RNA, not protein, expression. Our copy does not report these findings for pericytes or examine NRP1, CD147, or integrin α5β1. (LLM, conf=0.90)
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- Authors
- Yang, J., Chen, T., & Zhou, Y.
- Affiliations
- First Affiliated Hospital of Soochow University (CN)
- Soochow University (CN)
- Corresponding author
- Chen, Tan
- Zhou, Yafeng
- ORCID
- Zhou, Yafeng
- Venue
- Hereditas
- Published
- 2021-01-04
- Volume
- 158
- Issue
- 1
- Pages
- 4-4
- ISSN
- 0018-0661 (ISSN-L)
- 1601-5223
- PMC
- PMC7781406
- OpenAlex
- W3119560279
- Cited by
- 35
- References
- 22
- Citations by year
- 2025: 2 · 2024: 9 · 2023: 8 · 2022: 6 · 2021: 10
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Hereditas (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (81873486)
- Topics
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
- Keywords
- SARS-CoV-2, COVID-19 pandemic, cardiomyocytes, ACE2, TMPRSS2, cathepsin B, cathepsin L, viral entry, cardiac injury, single-cell RNA sequencing, human embryonic heart, cardiac conduction, mitochondrial respiratory chain, adrenergic signaling
- MeSH terms
- Angiotensin-Converting Enzyme 2, COVID-19, SARS-CoV-2, Cathepsin B, Heart, Humans, Serine Endopeptidases, Signal Transduction, Gene Expression Regulation, Developmental, Myocytes, Cardiac, Cathepsin L, Pandemics, Single-Cell Analysis, Gene Ontology
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