ArticleInternational journal of cardiology2022
SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress.
Article in International journal of cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Cardiovascular Disease as a Risk Amplifier of COVID-19 Severity and a Potential Correlations to Long-Term Gastrointestinal Sequelae.Journal of racial and ethnic health disparities · 2026Article
- Myocardial and Vascular Involvement in COVID-19 and Post-Vaccination States: Understanding Injury Pathways and Clinical Implications.Life (Basel, Switzerland) · 2026Review
- The regulatory mechanisms and translational applications of non-coding RNA in SARS-CoV-2 infection-related cardiovascular pathology.Frontiers in cardiovascular medicine · 2026Review
- A survey of SARS-CoV-2 tropism.Infectious diseases & immunity · 2025Review
- Diabetic cardiomyopathy and COVID-19: intersecting pathways and amplified cardiovascular risk.Frontiers in pharmacology · 2025Review
- The emerging role of heart-on-a-chip systems in delineating mechanisms of SARS-CoV-2-induced cardiac dysfunction.Bioengineering & translational medicine · 2024Review
- Decoding HiPSC-CM's Response to SARS-CoV-2: mapping the molecular landscape of cardiac injury.BMC genomics · 2024Article
- Beyond acute infection: molecular mechanisms underpinning cardiovascular complications in long COVID.Frontiers in cardiovascular medicine · 2024Review
- Transcriptome and machine learning analysis of the impact of COVID-19 on mitochondria and multiorgan damage.PloS one · 2024Article
- Pathophysiological involvement of host mitochondria in SARS-CoV-2 infection that causes COVID-19: a comprehensive evidential insight.Molecular and cellular biochemistry · 2023Review
- Impaired VEGF-A-Mediated Neurovascular Crosstalk Induced by SARS-CoV-2 Spike Protein: A Potential Hypothesis Explaining Long COVID-19 Symptoms and COVID-19 Vaccine Side Effects?Microorganisms · 2022Review
Corrections and comments
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Authors and funding
27 authors at 10 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe respiratory illness triggered by severe acute respiratory syndrome virus-2 (SARS-CoV-2) is often particularly serious or fatal amongst patients with pre-existing heart conditions. Although the mechanisms underlying SARS-CoV-2-related cardiac damage remain elusive, inflammation (i.e. 'cytokine storm') and oxidative stress are likely involved. METHODS AND
resultsHere we sought to determine: 1) if cardiomyocytes are targeted by SARS-CoV-2 and 2) how inflammation and oxidative stress promote the viral entry into cardiac cells. We analysed pro-inflammatory and oxidative stress and its impact on virus entry and virus-associated cardiac damage from SARS-CoV-2 infected patients and compared it to left ventricular myocardial tissues obtained from non-infected transplanted hearts either from end stage heart failure or non-failing hearts (donor group). We found that neuropilin-1 potentiates SARS-CoV-2 entry into human cardiomyocytes, a phenomenon driven by inflammatory and oxidant signals. These changes accounted for increased proteases activity and apoptotic markers thus leading to cell damage and apoptosis.
conclusionThis study provides new insights into the mechanisms of SARS-CoV-2 entry into the heart and defines promising targets for antiviral interventions for COVID-19 patients with pre-existing heart conditions or patients with co-morbidities.
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