ArticleNature communications2023
Timing and cell specificity of senescence drives postnatal lung development and injury.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
40 citing papers in PubMed, 41 citations in OpenAlex.
- Improving early risk stratification for bronchopulmonary Dysplasia in preterm infants using machine learning: development and external validation.Annals of medicine · 2026Article
- Angiogenesis in Lung Regeneration and Aging.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Neonatal hyperoxia promotes macrophage senescence and lung injury via a p38MAPK-dependent secretome.American journal of respiratory cell and molecular biology · 2026Article
- Prenatal cannabinoid and nicotine exposure: senescence as a developmental origin of bronchopulmonary dysplasia?Pediatric research · 2026Article
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Targeting Hyperoxia-Induced Cellular Senescence in Developing Human Airway Cells: Senomorphics Versus Senolytics Versus Antioxidants.Aging cell · 2026Article
- Neonatal Hyperoxia Induces Metabolic Reprogramming in Senescent Alveolar Macrophages, Leading to Persistent Lung Injury.Frontiers in bioscience (Landmark edition) · 2026Article
- Context-Dependent Roles of ANGPTL2-Mediated Inflammaging in Tissue Homeostasis, Pathological Tissue Remodeling, and Longevity.Aging cell · 2026Article
- Unfolded protein response in bronchopulmonary dysplasia: mechanisms, pathways, and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Role of connexin 43 in hyperoxia-induced bronchopulmonary dysplasia and associated pulmonary hypertension.PloS one · 2026Article
- Low hyper-oxygen exposure induces p21-dependent p53-independent senescence in alveolar cells.International journal of medical sciences · 2026Article
- An automated morphometric approach to evaluate distal lung patterning in mouse models of bronchopulmonary dysplasia.PloS one · 2026Article
- Hyperoxia promotes bronchopulmonary dysplasia via Noggin-mediated BMP4 antagonism and cellular senescence.Frontiers in physiology · 2026Article
- From development to regeneration: the endothelial interface in lung injury and repair.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- p53 maintains lineage fidelity during lung capillary injury-repair in neonatal hyperoxia.JCI insight · 2025Article
- Senescent Microglia Mediate Neuroinflammation-Induced Cognitive Dysfunction by Selective Elimination of Excitatory Synapses in the Hippocampal CA1.Aging cell · 2025Article
- Senescence at the Crossroads of Lung Development and Injury.American journal of respiratory cell and molecular biology · 2025Article
- Elevated Senescence Markers in Developing Trisomy 21 Human Lungs.American journal of respiratory cell and molecular biology · 2025Article
- Genetic variation in the activity of a TREM2-p53 signaling axis determines oxygen-induced lung injury.Nature immunology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Senescence causes age-related diseases and stress-related injury. Paradoxically, it is also essential for organismal development. Whether senescence contributes to lung development or injury in early life remains unclear. Here, we show that lung senescence occurred at birth and decreased throughout the saccular stage in mice. Reducing senescent cells at this stage disrupted lung development. In mice (<12 h old) exposed to hyperoxia during the saccular stage followed by air recovery until adulthood, lung senescence increased particularly in type II cells and secondary crest myofibroblasts. This peaked during the alveolar stage and was mediated by the p53/p21 pathway. Decreasing senescent cells during the alveolar stage attenuated hyperoxia-induced alveolar and vascular simplification. Conclusively, early programmed senescence orchestrates postnatal lung development whereas later hyperoxia-induced senescence causes lung injury through different mechanisms. This defines the ontogeny of lung senescence and provides an optimal therapeutic window for mitigating neonatal hyperoxic lung injury by inhibiting senescence.
Indexed as
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.