ArticleJournal of translational medicine2024
Communication between alveolar macrophages and fibroblasts via the TNFSF12-TNFRSF12A pathway promotes pulmonary fibrosis in severe COVID-19 patients.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Lung scRNA-seq reveals chronic inflammation and emphysemous phenotype in mice with osteogenesis imperfecta.Frontiers in genetics · 2026Article
- Over-Expression of TNFRSF12A Promotes Immune Suppression and Facilitates Angiogenesis in Triple-Negative Breast Cancer.Biology · 2025Article
- Hematologic and Immunologic Overlap Between COVID-19 and Idiopathic Pulmonary Fibrosis.Journal of clinical medicine · 2025Review
- Myeloid-Derived Suppressor Cell Accumulation Drives Intestinal Fibrosis through mCCL6/hCCL15 Chemokine-Mediated Fibroblast Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Transcriptome analysis of classical blood cells reveals downregulation of pro-inflammatory genes in the classical monocytes of long COVID patients.Frontiers in immunology · 2025Article
- Overlapping Systemic Proteins in COVID-19 and Lung Fibrosis Associated with Tissue Remodeling and Inflammation.Biomedicines · 2024Article
- Co-culture of human AT2 cells with fibroblasts reveals a MUC5B phenotype: insights from an organoid model.Molecular medicine (Cambridge, Mass.) · 2024Article
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Authors and funding
5 authors.
Funding
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Abstract
backgroundSevere COVID-19 infection has been associated with the development of pulmonary fibrosis, a condition that significantly affects patient prognosis. Understanding the underlying cellular communication mechanisms contributing to this fibrotic process is crucial.
objectiveIn this study, we aimed to investigate the role of the TNFSF12-TNFRSF12A pathway in mediating communication between alveolar macrophages and fibroblasts, and its implications for the development of pulmonary fibrosis in severe COVID-19 patients.
methodsWe conducted single-cell RNA sequencing (scRNA-seq) analysis using lung tissue samples from severe COVID-19 patients and healthy controls. The data was processed, analyzed, and cell types were annotated. We focused on the communication between alveolar macrophages and fibroblasts and identified key signaling pathways. In vitro experiments were performed to validate our findings, including the impact of TNFRSF12A silencing on fibrosis reversal.
resultsOur analysis revealed that in severe COVID-19 patients, alveolar macrophages communicate with fibroblasts primarily through the TNFSF12-TNFRSF12A pathway. This communication pathway promotes fibroblast proliferation and expression of fibrotic factors. Importantly, silencing TNFRSF12A effectively reversed the pro-proliferative and pro-fibrotic effects of alveolar macrophages.
conclusionThe TNFSF12-TNFRSF12A pathway plays a central role in alveolar macrophage-fibroblast communication and contributes to pulmonary fibrosis in severe COVID-19 patients. Silencing TNFRSF12A represents a potential therapeutic strategy for mitigating fibrosis in severe COVID-19 lung disease.
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