ReviewQJM : monthly journal of the Association of Physicians2023
Potential mechanisms for lung fibrosis associated with COVID-19 infection.
Review in QJM : monthly journal of the Association of Physicians, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
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
25 citing papers in PubMed, 29 citations in OpenAlex.
- Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026Review
- The PPAR-gamma agonist pioglitazone alleviates bleomycin-induced lung fibrosis in male BALB/c mice.Multidisciplinary respiratory medicine · 2026Article
- Circulating angiogenic progenitor cell apoptosis in Post-COVID-19 syndrome.International journal of cardiology. Heart & vasculature · 2026Article
- Serum lipidome remodeling in viral pneumonia: from pathophysiology to therapeutics.Frontiers in immunology · 2026Review
- The Central Role of Macrophages in Long COVID Pathophysiology.International journal of molecular sciences · 2025Review
- Decoding fibrosis in nonresolvable COVID-19: a role for myeloid-specific HIF1A deletion.American journal of physiology. Cell physiology · 2025Article
- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Long COVID and Its Impacts: A Case-Control Study in Brazil.Biomedicines · 2025Article
- Targeted immunotherapy rescues pulmonary fibrosis by reducing activated fibroblasts and regulating alveolar cell profile.Nature communications · 2025Article
- Respiratory long COVID in aged hamsters features impaired lung function post-exercise with bronchiolization and fibrosis.Nature communications · 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
- Equivocating and Deliberating on the Probability of COVID-19 Infection Serving as a Risk Factor for Lung Cancer and Common Molecular Pathways Serving as a Link.Pathogens (Basel, Switzerland) · 2024Review
- Article
- Unveiling the Pathological Mechanisms of Death Induced by SARS-CoV-2 Viral Pneumonia.Microorganisms · 2024Article
- Wogonin protects against bleomycin-induced mouse pulmonary fibrosis via the inhibition of CDK9/p53-mediated cell senescence.Frontiers in pharmacology · 2024Article
- Proximal immune-epithelial progenitor interactions drive chronic tissue sequelae post COVID-19.Research square · 2023Article
- Proximal immune-epithelial progenitor interactions drive chronic tissue sequelae post COVID-19.bioRxiv : the preprint server for biology · 2023Article
- The Effects of Vaccines on the Sequelae Rates of Recurrent Infections and the Severity of Pulmonary COVID-19 Infection by Imaging.Vaccines · 2023Article
- Senescence of alveolar epithelial progenitor cells: a critical driver of lung fibrosis.American journal of physiology. Cell physiology · 2023Review
- Maladaptive TGF-β Signals to the Alveolar Epithelium Drive Fibrosis after COVID-19 Infection.American journal of respiratory and critical care medicine · 2023Article
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 1 institution in 1 country.
Funding
Abstract
Pulmonary fibrosis is a sequelae of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection that currently lacks effective preventative or therapeutic measures. Post-viral lung fibrosis due to SARS-CoV-2 has been shown to be progressive on selected patients using imaging studies. Persistent infiltration of macrophages and monocytes, a main feature of SARS-CoV-2 pulmonary fibrosis, and long-lived circulating inflammatory monocytes might be driving factors promoting the profibrotic milieu in the lung. The upstream signal(s) that regulates the presence of these immune cells (despite complete viral clearance) remains to be explored. Current data indicate that much of the stimulating signals are localized in the lungs. However, an ongoing low-grade systemic inflammation in long Coronavirus Disease 2019 (COVID-19) symptoms suggests that certain non-pulmonary regulators such as epigenetic changes in hematopoietic stem cells might be critical to the chronic inflammatory response. Since nearly one-third of the world population have been infected, a timely understanding of the underlying pathogenesis leading to tissue remodeling is required. Herein, we review the potential pathogenic mechanisms driving lung fibrosis following SARS-CoV-2 infection based upon available studies and our preliminary findings (Graphical abstract).
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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.