ArticlePPAR research2012
PPARγ Signaling Mediates the Evolution, Development, Homeostasis, and Repair of the Lung.
Article in PPAR research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 80 citations in OpenAlex.
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- Understanding myofibroblast origin in the fibrotic lung.Chinese medical journal pulmonary and critical care medicine · 2024Review
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- Pulmonary Fibrosis and Diabetes Mellitus: Two coins with the same face.Archives of internal medicine research · 2024Article
- Simvastatin Improves Benign Prostatic Hyperplasia: Role of Peroxisome-Proliferator-Activated Receptor-γ and Classic WNT/β-Catenin Pathway.International journal of molecular sciences · 2023Article
- Daily Intraperitoneal Administration of Rosiglitazone Does Not Improve Lung Function or Alveolarization in Preterm Rabbits Exposed to Hyperoxia.Pharmaceutics · 2022Article
- PGC-1α activity and mitochondrial dysfunction in preterm infants.Frontiers in physiology · 2022Review
- Oxidative Stress and Respiratory Diseases in Preterm Newborns.International journal of molecular sciences · 2021Review
- The Parathyroid Hormone-Related Protein/Parathyroid Hormone 1 Receptor Axis in Adipose Tissue.Biomolecules · 2021Review
- MicroRNA Signatures Associated with Bronchopulmonary Dysplasia Severity in Tracheal Aspirates of Preterm Infants.Biomedicines · 2021Article
- From Clones to Buds and Branches: The Use of Lung Organoids to Model Branching MorphogenesisFrontiers in cell and developmental biology · 2021Review
- Interaction of Severe Acute Respiratory Syndrome Coronavirus 2 and Diabetes.Frontiers in endocrinology · 2021Review
- Cross-Talk Between Inflammation and Fibroblast Growth Factor 10 During Organogenesis and Pathogenesis: Lessons Learnt From the Lung and Other Organs.Frontiers in cell and developmental biology · 2021Review
- Antenatal PPAR-γ agonist pioglitazone stimulates fetal lung maturation equally in males and females.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Recombinant adiponectin protects the newborn rat lung from lipopolysaccharide-induced inflammatory injury.Physiological reports · 2020Article
- Developmental Timing Determines the Protective Effect of Maternal Electroacupuncture on Perinatal Nicotine Exposure-Induced Offspring Lung Phenotype.BioMed research international · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Epithelial-mesenchymal interactions mediated by soluble growth factors determine the evolution of vertebrate lung physiology, including development, homeostasis, and repair. The final common pathway for all of these positively adaptive properties of the lung is the expression of epithelial parathyroid-hormone-related protein, and its binding to its receptor on the mesenchyme, inducing PPARγ expression by lipofibroblasts. Lipofibroblasts then produce leptin, which binds to alveolar type II cells, stimulating their production of surfactant, which is necessary for both evolutionary and physiologic adaptation to atmospheric oxygen from fish to man. A wide variety of molecular insults disrupt such highly evolved physiologic cell-cell interactions, ranging from overdistention to oxidants, infection, and nicotine, all of which predictably cause loss of mesenchymal peroxisome-proliferator-activated receptor gamma (PPARγ) expression and the transdifferentiation of lipofibroblasts to myofibroblasts, the signature cell type for lung fibrosis. By exploiting such deep cell-molecular functional homologies as targets for leveraging lung homeostasis, we have discovered that we can effectively prevent and/or reverse the deleterious effects of these pathogenic agents, demonstrating the utility of evolutionary biology for the prevention and treatment of chronic lung disease. By understanding mechanisms of health and disease as an evolutionary continuum rather than as dissociated processes, we can evolve predictive medicine.
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.