ArticleNature cardiovascular research2024
CCL2-mediated endothelial injury drives cardiac dysfunction in long COVID.
Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
The trial behind it
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Who cites it
19 citing papers in PubMed.
- Generation of two homozygous iPSC lines carrying variants of uncertain significance in LMNA associated with cardiomyopathy.Stem cell research · 2026Article
- Spike 1 protein of SARS-CoV-2 induces endothelial inflammation and vascular dysfunction through interferon ISG15-dependent mechanisms.Cardiovascular research · 2026Article
- SARS-CoV-2 Persistence and Cardiovascular Sequelae in the Post-COVID Era: A Public Health Microbiology Perspective on Sudden Cardiac Death and Pulmonary Thromboembolism.Microorganisms · 2026Review
- Emerging biomodels to understand the pathophysiology of sepsis and evaluate new therapeutic strategies targeting extracellular histones.Materials today. Bio · 2026Review
- Vascularized Cardiac Tissue Engineering: From Advances in Biofabrication to Translational Applications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- SARS-CoV-2 reinfections and subsequent risk of hospital-diagnosed post-acute sequelae in Denmark (2020-2022): a nationwide cohort study.The Lancet regional health. Europe · 2026Article
- Toosendanin enhances endothelial repair and prevents inflammation via E2F1 mediated LINC01089.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Distinct Endothelial Phenotype Associates with Macrophage-Enriched Microenvironments in Triple-Negative Breast Cancer.Research square · 2026Article
- Virus-induced endothelial senescence as a cause and driving factor for ME/CFS and long COVID: mediated by a dysfunctional immune system.Cell death & disease · 2026Review
- Endothelial cell, but not neutrophil, programmed cell death receptor-ligand 1 loss has a morbid impact on experimental murine shock/sepsis-induced lung injury.Frontiers in immunology · 2026Article
- Multiscale profiling of tyrosine kinase inhibitor cardiotoxicity reveals mechanosensitive ion channel PIEZO1 as cardioprotective.Science translational medicine · 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
- Differential Effects of Endothelial Cell- as opposed to Neutrophil-Lineage Restricted PD-L1 Gene Expression on Experimental Murine Shock/ Sepsis-Induced Lung Injury.Research square · 2025Article
- Integrative approaches in cardiac tissue engineering: Bridging cellular complexity to create accurate physiological models.iScience · 2025Review
- Cardio-Pulmonary Features of Long COVID: From Molecular and Histopathological Characteristics to Clinical Implications.International journal of molecular sciences · 2025Review
- Vasoprotective effects of lysophosphatidic acid inhibit vascular injury caused by SARS-CoV-2 infection.Scientific reports · 2025Article
- Macrophage Containing Cardiac Organoids for Studying Inflammatory Programmes Driving Cardiovascular Disease.Current cardiology reports · 2025Review
- Generation of induced pluripotent stem cell line from a patient with long COVID.Stem cell research · 2025Article
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
Evidence linking the endothelium to cardiac injury in long coronavirus disease (COVID) is well documented, but the underlying mechanisms remain unknown. Here we show that cytokines released by endothelial cells (ECs) contribute to long-COVID-associated cardiac dysfunction. Using thrombotic vascular tissues from patients with long COVID and induced pluripotent stem cell-derived ECs (iPSC-ECs), we modeled endotheliitis and observed similar dysfunction and cytokine upregulation, notably CCL2. Cardiac organoids comprising iPSC-ECs and iPSC-derived cardiomyocytes showed cardiac dysfunction after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) exposure, driven by CCL2. Profiling of chromatin accessibility and gene expression at a single-cell resolution linked CCL2 to 'phenotype switching' and cardiac dysfunction, validated by high-throughput proteomics. Disease modeling of cardiac organoids and exposure of human ACE2 transgenic mice to SARS-CoV-2 spike proteins revealed that CCL2-induced oxidative stress promoted post-translational modification of cardiac proteins, leading to cardiac dysfunction. These findings suggest that EC-released cytokines contribute to cardiac dysfunction in long COVID, highlighting the importance of early vascular health monitoring in patients with long COVID.
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Registered trials
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