ArticleNature medicine2016
Targeting of the pulmonary capillary vascular niche promotes lung alveolar repair and ameliorates fibrosis.
Article in Nature medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 167 papers.
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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.
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Who cites it
167 citing papers in PubMed, 284 citations in OpenAlex.
- Angiogenesis in Lung Regeneration and Aging.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Non-Resolving Repair in Idiopathic Pulmonary Fibrosis: From Failed Cellular Transitions to Architectural Lock-In.International journal of molecular sciences · 2026Review
- Endothelial Atypical Receptors for Chemoattractants in Lung Immune Surveillance.European journal of immunology · 2026Review
- Disruption of macrophage migration inhibitory factor signaling induces major tumor-associated macrophage phenotypes in human M2 macrophages.Molecular biomedicine · 2026Article
- Angiocrine factors in tumor microenvironment: bidirectional crosstalk, mechanistic insights, and therapeutic strategies.Journal of translational medicine · 2026Review
- Recent advances in pulmonary fibrosis: from lung surfactant to the immune connection.Respiratory research · 2026Review
- Macrophage SH3 domain‑containing GRB2‑like protein B1 is required for Rab7‑mediated mitophagy in inflammation during sea water drowning acute lung injury.International journal of molecular medicine · 2026Article
- Profibrotic macrophage populations and cell communications in pulmonary fibrosis.Journal of physiology and biochemistry · 2026Review
- From Heterogeneity to Plasticity: Endothelial Dynamics in Lung Disease.Pulmonary circulation · 2026Review
- Inactivation Rap2a in Endothelial Cell Prevents Pulmonary Fibrosis by Regulating Immune Microenvironment Through MAP4K4-VCAM1 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Single-cell multiomics uncovers an endothelial mechanosensitive PIEZO1-IL-33 axis driving pulmonary fibrosis.Nature communications · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Extracellular vesicles from alveolar macrophages promotes pulmonary fibrosis through suppression of lung alveolar regeneration.Journal of nanobiotechnology · 2026Article
- Single-cell RNA sequencing elucidates potential mechanisms of endothelial cells in lung region-specific repair and remodeling in combined pulmonary fibrosis and emphysema.Respiratory research · 2026Article
- The Endothelial Cell Perspective in Pulmonary Fibrosis: From Cell Fate Decisions, Intercellular Communication, and EndoMT to Emerging Therapies.Canadian respiratory journal · 2026Review
- Source-renewing ectopic ApoB-TRL lipolysis in non-resolving ARDS: a testable spatial hypothesis.Frontiers in immunology · 2026Article
- von Willebrand Factor: An Unhealthy Bond between Lung Endothelium and Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Pulmonary Fibrosis-Focusing on the Future: Aspen Lung Conference 2024 Summary.American journal of respiratory cell and molecular biology · 2025Article
- Distal lung organoids derived from adult stem cells as novel tools in deciphering mechanisms of lung regeneration, infection, and cancer.Stem cells translational medicine · 2025Review
- Brain macrophages and pial fibroblasts promote inflammation in a hypomyelination model.Acta neuropathologica communications · 2025Article
107 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Although the lung can undergo self-repair after injury, fibrosis in chronically injured or diseased lungs can occur at the expense of regeneration. Here we study how a hematopoietic-vascular niche regulates alveolar repair and lung fibrosis. Using intratracheal injection of bleomycin or hydrochloric acid in mice, we show that repetitive lung injury activates pulmonary capillary endothelial cells (PCECs) and perivascular macrophages, impeding alveolar repair and promoting fibrosis. Whereas the chemokine receptor CXCR7, expressed on PCECs, acts to prevent epithelial damage and ameliorate fibrosis after a single round of treatment with bleomycin or hydrochloric acid, repeated injury leads to suppression of CXCR7 expression and recruitment of vascular endothelial growth factor receptor 1 (VEGFR1)-expressing perivascular macrophages. This recruitment stimulates Wnt/β-catenin-dependent persistent upregulation of the Notch ligand Jagged1 (encoded by Jag1) in PCECs, which in turn stimulates exuberant Notch signaling in perivascular fibroblasts and enhances fibrosis. Administration of a CXCR7 agonist or PCEC-targeted Jag1 shRNA after lung injury promotes alveolar repair and reduces fibrosis. Thus, targeting of a maladapted hematopoietic-vascular niche, in which macrophages, PCECs and perivascular fibroblasts interact, may help to develop therapy to spur lung regeneration and alleviate fibrosis.
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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.