ArticleStem cell reports2021
Cardiomyocytes recruit monocytes upon SARS-CoV-2 infection by secreting CCL2.
Article in Stem cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- Systems biology analysis reveals miRNA-mRNA networks associated with cardiomyocyte responses to SARS-CoV-2 infection.NPJ systems biology and applications · 2026Article
- SARS-CoV-2-infected cardiomyocytes exhibit upregulated necroptosis, but no evidence of mitochondrial permeability transition.Journal of molecular and cellular cardiology plus · 2026Article
- Innate immune activation and mitochondrial ROS induce acute and persistent cardiac conduction system dysfunction after COVID-19.JCI insight · 2025Article
- Decoding long COVID-associated cardiovascular dysfunction: Mechanisms, models, and new approach methodologies.Journal of molecular and cellular cardiology · 2025Review
- Organoids in respiratory virus research: advances and perspectives.Molecular biomedicine · 2025Review
- APOE genotype confers context-dependent neurovascular vulnerability in immune-vascularized human forebrain organoids.bioRxiv : the preprint server for biology · 2025Article
- Review
- Immune modulation: the key to combat SARS-CoV-2 induced myocardial injury.Frontiers in immunology · 2025Review
- Chemokine CCL2 and its receptor CCR2 in different age groups of patients with COVID-19.BMC immunology · 2024Article
- The emerging role of heart-on-a-chip systems in delineating mechanisms of SARS-CoV-2-induced cardiac dysfunction.Bioengineering & translational medicine · 2024Review
- The inflammatory spectrum of cardiomyopathies.Frontiers in cardiovascular medicine · 2024Review
- COVID-19: a multi-organ perspective.Frontiers in cellular and infection microbiology · 2024Review
- RNA m5C methylation modification: a potential therapeutic target for SARS-CoV-2-associated myocarditis.Frontiers in immunology · 2024Review
- Possible mechanisms of SARS-CoV-2-associated myocardial fibrosis: reflections in the post-pandemic era.Frontiers in microbiology · 2024Review
- Sex differences in the cardiac stress response following SARS-CoV-2 infection of ferrets.American journal of physiology. Heart and circulatory physiology · 2023Article
- Mechanism of COVID-19-Induced Cardiac Damage from Patient, In Vitro and Animal Studies.Current heart failure reports · 2023Review
- Microfluidic Organ-Chips and Stem Cell Models in the Fight Against COVID-19.Circulation research · 2023Review
- More than a key-the pathological roles of SARS-CoV-2 spike protein in COVID-19 related cardiac injury.Sports medicine and health science · 2023Review
- Associations between Periodontitis, COVID-19, and Cardiometabolic Complications: Molecular Mechanisms and Clinical Evidence.Metabolites · 2022Review
- Role of CCL2/CCR2 axis in the pathogenesis of COVID-19 and possible Treatments: All options on the Table.International immunopharmacology · 2022Review
Corrections and comments
- Erratum issued
- Update of
Authors and funding
26 authors at 5 institutions in 1 country.
Funding
Abstract
Heart injury has been reported in up to 20% of COVID-19 patients, yet the cause of myocardial histopathology remains unknown. Here, using an established in vivo hamster model, we demonstrate that SARS-CoV-2 can be detected in cardiomyocytes of infected animals. Furthermore, we found damaged cardiomyocytes in hamsters and COVID-19 autopsy samples. To explore the mechanism, we show that both human pluripotent stem cell-derived cardiomyocytes (hPSC-derived CMs) and adult cardiomyocytes (CMs) can be productively infected by SARS-CoV-2, leading to secretion of the monocyte chemoattractant cytokine CCL2 and subsequent monocyte recruitment. Increased CCL2 expression and monocyte infiltration was also observed in the hearts of infected hamsters. Although infected CMs suffer damage, we find that the presence of macrophages significantly reduces SARS-CoV-2-infected CMs. Overall, our study provides direct evidence that SARS-CoV-2 infects CMs in vivo and suggests a mechanism of immune cell infiltration and histopathology in heart tissues of COVID-19 patients.
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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.