ArticleScience translational medicine2021
Lung epithelial and endothelial damage, loss of tissue repair, inhibition of fibrinolysis, and cellular senescence in fatal COVID-19.
Article in Science translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.
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The trial behind it
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Who cites it
155 citing papers in PubMed, 244 citations in OpenAlex.
- Phase I/II clinical trial of efficacy and safety of EGCG oxygen nebulization inhalation in the treatment of COVID-19 pneumonia patients with cancer.BMC cancer · 2024Trial
- The role of alveolar epithelial junctions in early lung injury and COVID-19-induced fibrosis.Histochemistry and cell biology · 2026Article
- Precision nanomedicine for pulmonary diseases: from molecular targeting to clinical translation.Signal transduction and targeted therapy · 2026Review
- SARS-CoV-2 drives upregulation of EpCAM in respiratory epithelial cells with hypercellular profile during severe COVID-19.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Early Immunological Biomarkers for Personalized Treatment Selection in Severe COVID-19: Post Hoc Machine Learning Analysis of a Randomized Clinical Trial.JMIR medical informatics · 2026Article
- Risk Factors for Barotrauma with Extra-Alveolar Air in a Selected COVID-19 Patient Population: Experience from a Tertiary University Hospital.Journal of clinical medicine · 2026Article
- Renin-angiotensin imbalance promotes excessive fibrin deposition through M2 macrophage-derived tissue factor expression in eosinophilic chronic rhinosinusitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Associations between respiratory diseases and lung cancer risk: a secondary analysis of the large-scale prospective UK biobank cohort.BMJ open respiratory research · 2026Article
- Fluid Balance is Associated with Differential Effects on Respiratory Failure between Critically Ill and Noncritically Ill Adults with SARS-CoV-2: a Retrospective Cohort Study.Shock (Augusta, Ga.) · 2026Article
- SARS-CoV-2 nonspike structural proteins hijack mucosa epithelial cell fate.Cell death & disease · 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
- The Unexpected Protective Role of Thrombosis in Lung Injury via Endothelial Alox15.Circulation research · 2026Article
- Targeting gasdermin D-mediated pyroptosis: a precision anti-inflammatory strategy for acute and chronic lung diseases.Inflammopharmacology · 2026Review
- The Extracellular Matrix and the Immune System in Acute Lung Injury: Partners in Damage and Repair.Biomedicines · 2025Review
- Integrative multi-omics framework for causal gene discovery in Long COVID.PLoS computational biology · 2025Article
- RBMX2 linkseLife · 2025Article
- Putrescine functions as a metabolic checkpoint in replication stress-induced senescence.Cellular and molecular life sciences : CMLS · 2025Article
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- An RGD motif on SARS-CoV-2 Spike induces TGF-β signaling and downregulates interferon.Journal of virology · 2025Article
- A Human Immuno-Lung Organoid Model to Study Macrophage-Mediated Lung Cell Senescence Upon SARS-CoV-2 Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
95 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
28 authors at 12 institutions in 1 country.
Funding
Abstract
Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is characterized by respiratory distress, multiorgan dysfunction, and, in some cases, death. The pathological mechanisms underlying COVID-19 respiratory distress and the interplay with aggravating risk factors have not been fully defined. Lung autopsy samples from 18 patients with fatal COVID-19, with symptom onset-to-death times ranging from 3 to 47 days, and antemortem plasma samples from 6 of these cases were evaluated using deep sequencing of SARS-CoV-2 RNA, multiplex plasma protein measurements, and pulmonary gene expression and imaging analyses. Prominent histopathological features in this case series included progressive diffuse alveolar damage with excessive thrombosis and late-onset pulmonary tissue and vascular remodeling. Acute damage at the alveolar-capillary barrier was characterized by the loss of surfactant protein expression with injury to alveolar epithelial cells, endothelial cells, respiratory epithelial basal cells, and defective tissue repair processes. Other key findings included impaired clot fibrinolysis with increased concentrations of plasma and lung plasminogen activator inhibitor-1 and modulation of cellular senescence markers, including p21 and sirtuin-1, in both lung epithelial and endothelial cells. Together, these findings further define the molecular pathological features underlying the pulmonary response to SARS-CoV-2 infection and provide important insights into signaling pathways that may be amenable to therapeutic intervention.
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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.