ArticleCardiovascular research2023
The pulmonary vasculature in lethal COVID-19 and idiopathic pulmonary fibrosis at single-cell resolution.
Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- From Heterogeneity to Plasticity: Endothelial Dynamics in Lung Disease.Pulmonary circulation · 2026Review
- Endothelial Heterogeneity in Pulmonary Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- S100A8Frontiers in immunology · 2026Article
- Article
- Elevated Systemic Immune-Inflammation Index is Associated with Gestational Diabetes Mellitus: A Multicenter Retrospective Studies.Journal of inflammation research · 2026Article
- The Endothelial Cell Perspective in Pulmonary Fibrosis: From Cell Fate Decisions, Intercellular Communication, and EndoMT to Emerging Therapies.Canadian respiratory journal · 2026Review
- Integrated Mendelian Randomization and Single-Cell RNA Sequencing Analyses Reveal Lactate Metabolism as a Key Pathway in COVID-19-Induced Pulmonary Fibrosis.Canadian respiratory journal · 2026Article
- Idiopathic Pulmonary Fibrosis: Cellular Heterogeneity, Mechanisms, and Therapeutic Implications.MedComm · 2025Review
- SARS-CoV-2 enhances complement-mediated endothelial injury via the suppression of membrane complement regulatory proteins.Emerging microbes & infections · 2025Article
- Structure-guided design of nucleosome-inspired nanoparticles for overcoming pulmonary barriers in fibrotic lung gene therapy.Science advances · 2025Article
- Single-cell dissection of chronic lung allograft dysfunction reveals convergent and distinct fibrotic mechanisms.JCI insight · 2025Article
- Unveiling the secret of cellular metamorphosis: the crucial role of EndMT mechanisms in COVID-19-induced pulmonary fibrosis.Inflammopharmacology · 2025Review
- Aging affects reprogramming of pulmonary capillary endothelial cells after lung injury in male mice.Nature communications · 2025Article
- Hematopoietic loss of Y chromosome activates immune checkpoints and contributes to impaired senescent cell clearance and renal disease.Science translational medicine · 2025Article
- SARS-CoV-2 uptake and inflammatory response in senescent endothelial cells are regulated by the BSG/VEGFR2 pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Hematologic and Immunologic Overlap Between COVID-19 and Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 2025Review
- Mosaic loss of chromosome Y in blood is associated with male susceptibility for idiopathic pulmonary fibrosis.Communications medicine · 2025Article
- Single-cell transcriptomic analysis deciphers the inflammatory microenvironment characterized by CXCL9+ fibroblasts and ACKR1+ endothelial cells in immune-related myocarditis.Journal of translational medicine · 2025Article
- Pulmonary fibrosis: from mechanisms to therapies.Journal of translational medicine · 2025Review
- Ectopic Expansion of Pulmonary Vasculature in Fibrotic Lung Disease and Lung Adenocarcinoma Marked by Proangiogenic COL15A1+ Endothelial Cells.Pulmonary circulation · 2025Article
Corrections and comments
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Authors and funding
48 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsSevere acute respiratory syndrome coronavirus-2 infection causes COVID-19, which in severe cases evokes life-threatening acute respiratory distress syndrome (ARDS). Transcriptome signatures and the functional relevance of non-vascular cell types (e.g. immune and epithelial cells) in COVID-19 are becoming increasingly evident. However, despite its known contribution to vascular inflammation, recruitment/invasion of immune cells, vascular leakage, and perturbed haemostasis in the lungs of severe COVID-19 patients, an in-depth interrogation of the endothelial cell (EC) compartment in lethal COVID-19 is lacking. Moreover, progressive fibrotic lung disease represents one of the complications of COVID-19 pneumonia and ARDS. Analogous features between idiopathic pulmonary fibrosis (IPF) and COVID-19 suggest partial similarities in their pathophysiology, yet, a head-to-head comparison of pulmonary cell transcriptomes between both conditions has not been implemented to date. METHODS AND
resultsWe performed single-nucleus RNA-sequencing on frozen lungs from 7 deceased COVID-19 patients, 6 IPF explant lungs, and 12 controls. The vascular fraction, comprising 38 794 nuclei, could be subclustered into 14 distinct EC subtypes. Non-vascular cell types, comprising 137 746 nuclei, were subclustered and used for EC-interactome analyses. Pulmonary ECs of deceased COVID-19 patients showed an enrichment of genes involved in cellular stress, as well as signatures suggestive of dampened immunomodulation and impaired vessel wall integrity. In addition, increased abundance of a population of systemic capillary and venous ECs was identified in COVID-19 and IPF. COVID-19 systemic ECs closely resembled their IPF counterparts, and a set of 30 genes was found congruently enriched in systemic ECs across studies. Receptor-ligand interaction analysis of ECs with non-vascular cell types in the pulmonary micro-environment revealed numerous previously unknown interactions specifically enriched/depleted in COVID-19 and/or IPF.
conclusionsThis study uncovered novel insights into the abundance, expression patterns, and interactomes of EC subtypes in COVID-19 and IPF, relevant for future investigations into the progression and treatment of both lethal conditions.
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