ArticleHereditas2021
Mediators of SARS-CoV-2 entry are preferentially enriched in cardiomyocytes.
Article in Hereditas, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- SARS-CoV-2 damages cardiomyocyte mitochondria and implicates long COVID-associated cardiovascular manifestations.Journal of advanced research · 2026Article
- Article
- Cathepsin B in cardiovascular disease: Underlying mechanisms and therapeutic strategies.Journal of cellular and molecular medicine · 2024Review
- Severe pediatric COVID-19: a review from the clinical and immunopathophysiological perspectives.World journal of pediatrics : WJP · 2024Review
- Sympathetic remodeling and altered angiotensin-converting enzyme 2 localization occur in patients with cardiac disease but are not exacerbated by severe COVID-19.Autonomic neuroscience : basic & clinical · 2024Article
- Plasma miR-195-5p predicts the severity of Covid-19 in hospitalized patients.Scientific reports · 2023Article
- Review
- Parallel use of human stem cell lung and heart models provide insights for SARS-CoV-2 treatment.Stem cell reports · 2023Article
- COVID-19, Myocarditis and Pericarditis.Circulation research · 2023Review
- Network-Based Data Analysis Reveals Ion Channel-Related Gene Features in COVID-19: A Bioinformatic Approach.Biochemical genetics · 2023Article
- Organ manifestations of COVID-19: what have we learned so far (not only) from autopsies?Virchows Archiv : an international journal of pathology · 2022Review
- Interaction of SARS-CoV-2 with cardiomyocytes: Insight into the underlying molecular mechanisms of cardiac injury and pharmacotherapy.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Acute myocardial injury in patients with COVID-19: Possible mechanisms and clinical implications.World journal of clinical cases · 2022Review
- Molecular and cellular mechanisms involved in tissue-specific metabolic modulation by SARS-CoV-2.Frontiers in microbiology · 2022Review
- Prediction of binding miRNAs involved with immune genes to the SARS-CoV-2 by using sequence features extraction and One-class SVM.Informatics in medicine unlocked · 2022Article
- Cytokine storm in COVID-19: from viral infection to immune responses, diagnosis and therapy.International journal of biological sciences · 2022Review
- COVID-19, the Pandemic of the Century and Its Impact on Cardiovascular Diseases.Cardiology discovery · 2021Article
- Review
- SARS-CoV-2 infection initiates interleukin-17-enriched transcriptional response in different cells from multiple organs.Scientific reports · 2021Article
- Hypotheses and facts for genetic factors related to severe COVID-19.World journal of virology · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe 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.
resultsThe 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.
conclusionsOur 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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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.