ReviewAmerican journal of physiology. Lung cellular and molecular physiology2025
From development to regeneration: the endothelial interface in lung injury and repair.
Review in American journal of physiology. Lung cellular and molecular physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed.
- LATS1/2 inactivation drives a distinct venous endothelial cell response that contributes to fibrotic remodeling of the lung.Science advances · 2026Article
- Early-life lung injury and the developing brain: a lung-brain axis perspective on neurodevelopmental disorders.Journal of neuroinflammation · 2026Review
- Gut dysbiosis modulates hyperoxia-induced bronchopulmonary dysplasia by promoting EMT through activating TLR4/NF-κB pathway.Molecular medicine (Cambridge, Mass.) · 2026Article
- Beyond the epithelium: multicellular niches in lung regeneration and disease.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Alveolar macrophage-neutrophil crosstalk in acute lung injury: mechanisms, feedback loops, and therapeutic opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- The Lung-Kidney Axis: A Coordinated Regulation of Oxygen Sensing and Erythropoiesis.Biomedicines · 2026Review
- The single-cell immune atlas of bacterial pneumonia: from inflammatory cell infiltration to treatable cell states.Frontiers in cellular and infection microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
The pulmonary alveolar-capillary niche is a highly specialized interface that balances gas exchange with maintenance functions and repair. Advances in single cell transcriptomics have uncovered endothelial heterogeneity, which underlies developmental angiogenesis and plastic responses to injury. Emerging evidence from a neonatal hyperoxia model highlights CAP1 to CAP2 transitions and the role of p53 in maintaining lineage fidelity. Beyond intrinsic lineage plasticity, circulating mediators such as cell-free hemoglobin drive endothelial barrier disruption through oxidative injury and lipid modification. As new signaling pathways and therapeutics targets emerge, complementary strategies are being developed at the cellular level, including adoptive transfer of mesenchymal stromal and immune cells, although mechanisms of endothelial adhesion and homing remain incompletely defined. Finally, biomechanical forces such as shear stress have become critical contextual cues for endothelial signaling, yet remain underrepresented in some experimental models. Together, these insights underscore the central role of endothelial heterogeneity, injury responses, and environmental cues in shaping pulmonary vascular health and repair, with implications for designing targeted therapies in both pediatric and adult lung disease.
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Identifiers
What OpenQuestion holds
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.