ArticleRespiratory research2020
SARS-CoV-2 induces transcriptional signatures in human lung epithelial cells that promote lung fibrosis.
Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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
130 citing papers in PubMed, 1 synthesis or guideline pooled it, 203 citations in OpenAlex.
- The rationale for the treatment of long-Covid symptoms - A cardiologist's view.Frontiers in cardiovascular medicine · 2022Pooled it
- Vitronectin metabolically programs profibrotic macrophages in 3D cultures and idiopathic pulmonary fibrosis.Science advances · 2026Article
- A Rare Case of Pulmonary Ossification Findings That Rapidly Progressed and Improved During the Course of COVID-19 Pneumonia.Respirology case reports · 2026Article
- Combined use of serum KL-6 and respiratory functional parameters for identifying fibrotic lung damage in SARS-CoV-2-induced interstitial pneumonia.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2026Article
- Serum Mammalian Target of Rapamycin (mTOR) Levels in Patients with Post-COVID-19 Fibrotic-like Lung Changes: A Cross-Sectional Study.Diagnostics (Basel, Switzerland) · 2026Article
- The NLRP3 inflammasome as a key pathway in the affective and chronic fatigue symptoms of Long COVID.Journal of translational medicine · 2026Article
- Progress in the Application of Pirfenidone in Post-COVID-19 Pulmonary Fibrosis: A Review.Cureus · 2025Review
- TGF-β inhibitor SB431542 suppresses SARS-CoV-2 replication through multistep inhibition.Journal of virology · 2025Article
- The long reach of influenza and other respiratory viruses: from acute epithelial injury to post-viral lung disease.Clinical microbiology reviews · 2025Review
- Emerging Concepts in Therapeutic Interventions for Idiopathic Pulmonary Fibrosis.Seminars in respiratory and critical care medicine · 2025Review
- Inflammatory and Angiogenic Mediators Are Differentially Ex-Pressed in Patients with Post-COVID-19 Syndrome with Normal and Abnormal Spirometry Results.Healthcare (Basel, Switzerland) · 2025Article
- Article
- Vitronectin regulates lung tissue remodeling and emphysema in chronic obstructive pulmonary disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Postacute COVID-19 fatigue, dyspnea and reduced activity in children and adolescents.Pediatric research · 2025Article
- Impact of COVID-19 Pneumonia on Chest Computed Tomography Scan and Spirometry During Six Months.Medical journal of the Islamic Republic of Iran · 2025Article
- Increased circulating levels of SP-D and IL-10 are associated with the development of disease severity and pulmonary fibrosis in patients with COVID-19.Frontiers in immunology · 2025Article
- Revisiting pulmonary fibrosis: inflammatory dynamics of the lipofibroblast-to-inflammatory lipofibroblast-to-activated myofibroblast reversible switch.Frontiers in immunology · 2025Review
- KDDC: a new framework that integrates kmers, dataset filtering, dimension reduction and classification algorithms to achieve immune cell heterogeneity classification.Frontiers in immunology · 2025Article
- Convergent evolution in high-altitude and marine mammals: Molecular adaptations to pulmonary fibrosis and hypoxia.Zoological research · 2024Article
- Decoding the mechanism of Qingjie formula in the prevention of COVID-19 based on network pharmacology and molecular docking.Heliyon · 2024Article
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundSevere acute respiratory syndrome (SARS)-CoV-2-induced coronavirus disease-2019 (COVID-19) is a pandemic disease that affects > 2.8 million people worldwide, with numbers increasing dramatically daily. However, there is no specific treatment for COVID-19 and much remains unknown about this disease. Angiotensin-converting enzyme (ACE)2 is a cellular receptor of SARS-CoV-2. It is cleaved by type II transmembrane serine protease (TMPRSS)2 and disintegrin and metallopeptidase domain (ADAM)17 to assist viral entry into host cells. Clinically, SARS-CoV-2 infection may result in acute lung injury and lung fibrosis, but the underlying mechanisms of COVID-19 induced lung fibrosis are not fully understood.
methodsThe networks of ACE2 and its interacting molecules were identified using bioinformatic methods. Their gene and protein expressions were measured in human epithelial cells after 24 h SARS-CoV-2 infection, or in existing datasets of lung fibrosis patients.
resultsWe confirmed the binding of SARS-CoV-2 and ACE2 by bioinformatic analysis. TMPRSS2, ADAM17, tissue inhibitor of metalloproteinase (TIMP)3, angiotensinogen (AGT), transformation growth factor beta (TGFB1), connective tissue growth factor (CTGF), vascular endothelial growth factor (VEGF) A and fibronectin (FN) were interacted with ACE2, and the mRNA and protein of these molecules were expressed in lung epithelial cells. SARS-CoV-2 infection increased ACE2, TGFB1, CTGF and FN1 mRNA that were drivers of lung fibrosis. These changes were also found in lung tissues from lung fibrosis patients.
conclusionsTherefore, SARS-CoV-2 binds with ACE2 and activates fibrosis-related genes and processes to induce lung fibrosis.
Indexed as
Identifiers
What OpenQuestion holds
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.