ArticleNature communications2024
Vascular endothelial-derived SPARCL1 exacerbates viral pneumonia through pro-inflammatory macrophage activation.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Teneurins Are SPARCL1 Receptors.bioRxiv : the preprint server for biology · 2026Article
- Immune cell disorder in viral pneumonia.Journal of translational medicine · 2026Review
- Cumambrin B Alleviates Sepsis-Associated Acute Lung Injury by Activating the Nrf2/HO-1 Pathway.Biomedicines · 2026Article
- Palmitoylated COX-2Journal of advanced research · 2026Article
- Pathological neural and immune synapses in glioblastoma progression: mechanisms and therapeutic opportunities.Frontiers in neural circuits · 2026Review
- Immune-endothelial-coagulation crosstalk as a driver of multi-organ dysfunction in severe viral pneumonia.Frontiers in immunology · 2026Review
- Exploring the Role of SPARC in Atherosclerosis: Mechanisms and Potential Implications.Current atherosclerosis reports · 2025Review
- Scar wars: the viral menace.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Single-cell spatial atlas of smoking-induced changes in human gingival tissues.International journal of oral science · 2025Article
- Digital spatial profiling reveals the molecular signatures of BK virus infection in renal transplant recipients.Translational andrology and urology · 2025Article
- ZBP1-driven cell death in severe influenza.Trends in microbiology · 2025Review
- The lung microvasculature promotes alveolar type 2 cell differentiation via secreted SPARCL1.Stem cell reports · 2025Article
- Profile and clinical significance of SPARCL1 and its prognostic significance in breast cancer.Oncology letters · 2025Article
- Longitudinal single-cell profiles of lung regeneration after viral infection reveal persistent injury-associated cell states.Cell stem cell · 2025Article
- Specialized Pulmonary Vascular Cells in Development and Disease.Annual review of physiology · 2025Review
- Role of toll-like receptors in pulmonary immunity: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Serum legumain is a potential biomarker for community-acquired pneumonia: a prospective cohort study.International journal of medical sciences · 2025Article
- KCTD10 inhibits lung cancer metastasis and angiogenesis via ubiquitin-mediated β-catenin degradation.Frontiers in immunology · 2025Article
- The innate immune response in SARS-CoV2 infection: focus on toll-like receptor 4 in severe disease outcomes.Frontiers in immunology · 2025Review
- An injury-induced mesenchymal-epithelial cell niche coordinates regenerative responses in the lung.Science (New York, N.Y.) · 2024Article
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19 authors.
Funding
Abstract
Inflammation induced by lung infection is a double-edged sword, moderating both anti-viral and immune pathogenesis effects; the mechanism of the latter is not fully understood. Previous studies suggest the vasculature is involved in tissue injury. Here, we report that expression of Sparcl1, a secreted matricellular protein, is upregulated in pulmonary capillary endothelial cells (EC) during influenza-induced lung injury. Endothelial overexpression of SPARCL1 promotes detrimental lung inflammation, with SPARCL1 inducing 'M1-like' macrophages and related pro-inflammatory cytokines, while SPARCL1 deletion alleviates these effects. Mechanistically, SPARCL1 functions through TLR4 on macrophages in vitro, while TLR4 inhibition in vivo ameliorates excessive inflammation caused by endothelial Sparcl1 overexpression. Finally, SPARCL1 expression is increased in lung ECs from COVID-19 patients when compared with healthy donors, while fatal COVID-19 correlates with higher circulating SPARCL1 protein levels in the plasma. Our results thus implicate SPARCL1 as a potential prognosis biomarker for deadly COVID-19 pneumonia and as a therapeutic target for taming hyperinflammation in pneumonia.
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