ArticleNature communications2024
Lung injury-induced activated endothelial cell states persist in aging-associated progressive fibrosis.
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 49 papers.
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Who cites it
49 citing papers in PubMed.
- Vascular aging as a driver of organ dysfunction and systemic aging.Nature cardiovascular research · 2026Review
- Angiogenesis in Lung Regeneration and Aging.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- LATS1/2 inactivation drives a distinct venous endothelial cell response that contributes to fibrotic remodeling of the lung.Science advances · 2026Article
- Non-Resolving Repair in Idiopathic Pulmonary Fibrosis: From Failed Cellular Transitions to Architectural Lock-In.International journal of molecular sciences · 2026Review
- Airway administered artificial mitochondria-enriched nanovesicles for efficient and selective mitochondria transfer to intervene in pulmonary fibrosis.Nature communications · 2026Article
- Endothelial Atypical Receptors for Chemoattractants in Lung Immune Surveillance.European journal of immunology · 2026Review
- Article
- Multi-omics integration identifies macrophage senescence driven by the RUNX1-P53 axis as a key mechanism in diabetic foot ulcer.Functional & integrative genomics · 2026Article
- Does Tuberculosis Leave a Thromboinflammatory Memory After Cure? A Narrative Review with a Conceptual Framework on Hypercoagulability, Cellular Reservoirs, and Extracellular Vesicle Signaling.International journal of molecular sciences · 2026Review
- Liver sinusoidal endothelial cell fenestrations in metabolic liver disease: from molecular mechanisms to therapeutic perspectives.Cell communication and signaling : CCS · 2026Review
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Linking Genetic Risk to Disease-Relevant Cellular States via Metacell-Informed Modeling with ICePop.bioRxiv : the preprint server for biology · 2026Article
- Transcriptional landscape of pulmonary artery endothelium reveals subpopulation- and disease-specific remodeling signatures.Communications biology · 2026Article
- Treatment of pulmonary fibrosis: From disease mechanisms to future novel therapies (Review).International journal of molecular medicine · 2026Review
- Rebalancing the Neurovascular Axis: NTRK2 Isoform Equilibrium as a Determinant of Pulmonary Endothelial Regeneration.Cell proliferation · 2026Article
- 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
- Mechanisms of fibrotic tissue remodelling: insights from systemic sclerosis.Nature reviews. Rheumatology · 2026Review
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
Corrections and comments
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17 authors.
Funding
Abstract
Progressive lung fibrosis is associated with poorly understood aging-related endothelial cell dysfunction. To gain insight into endothelial cell alterations in lung fibrosis we performed single cell RNA-sequencing of bleomycin-injured lungs from young and aged mice. Analysis reveals activated cell states enriched for hypoxia, glycolysis and YAP/TAZ activity in ACKR1+ venous and TrkB+ capillary endothelial cells. Endothelial cell activation is prevalent in lungs of aged mice and can also be detected in human fibrotic lungs. Longitudinal single cell RNA-sequencing combined with lineage tracing demonstrate that endothelial activation resolves in young mouse lungs but persists in aged ones, indicating a failure of the aged vasculature to return to quiescence. Genes associated with activated lung endothelial cells states in vivo can be induced in vitro by activating YAP/TAZ. YAP/TAZ also cooperate with BDNF, a TrkB ligand that is reduced in fibrotic lungs, to promote capillary morphogenesis. These findings offer insights into aging-related lung endothelial cell dysfunction that may contribute to defective lung injury repair and persistent fibrosis.
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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.