ReviewAntioxidants & redox signaling2014
The lung alveolar lipofibroblast: an evolutionary strategy against neonatal hyperoxic lung injury.
Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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Who cites it
45 citing papers in PubMed, 63 citations in OpenAlex.
- BCL9 inhibition promotes fibroblast lipogenesis by regulating macrophage-fibroblast interactions to attenuate pulmonary fibrosis.Signal transduction and targeted therapy · 2026Article
- Rediscovering Lung Lipofibroblast: A Lipid Wizard on the Alveolar Fibroblast Spectrum.American journal of respiratory cell and molecular biology · 2026Article
- CAR-engineered cytolytic Tregs reverse pulmonary fibrosis and remodel the fibrotic niche with limited CRS.JCI insight · 2025Article
- Wnt Activation in Mature Dermal Adipocytes Leads to Lipodystrophy and Skin Fibrosis via ATGL-Dependent Lipolysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Evidence for a lipofibroblast-to-The European respiratory journal · 2025Article
- Revisiting pulmonary fibrosis: inflammatory dynamics of the lipofibroblast-to-inflammatory lipofibroblast-to-activated myofibroblast reversible switch.Frontiers in immunology · 2025Review
- Predictive value of serum MED1 and PGC-1α for bronchopulmonary dysplasia in preterm infants.BMC pulmonary medicine · 2024Observational
- Cell Cross-Talk in Alveolar Microenvironment: From Lung Injury to Fibrosis.American journal of respiratory cell and molecular biology · 2024Review
- Tissue fibrosis associated depletion of lipid-filled cells.Experimental dermatology · 2024Review
- Oxygen-driven divergence of marine group II archaea reflected by transitions of superoxide dismutases.Microbiology spectrum · 2024Article
- Oncogenic KRAS Drives Lipofibrogenesis to Promote Angiogenesis and Colon Cancer Progression.Cancer discovery · 2023Article
- Stem/Progenitor Cells and Related Therapy in Bronchopulmonary Dysplasia.International journal of molecular sciences · 2023Review
- Evidence of SARS-CoV-2 infection in postmortem lung, kidney, and liver samples, revealing cellular targets involved in COVID-19 pathogenesis.Archives of virology · 2023Article
- Caffeine reduces oxidative stress to protect against hyperoxia-induced lung injury via the adenosine A2A receptor/cAMP/PKA/Src/ERK1/2/p38MAPK pathway.Redox report : communications in free radical research · 2022Article
- Pulmonary Fibrosis as a Result of Acute Lung Inflammation: Molecular Mechanisms, Relevant In Vivo Models, Prognostic and Therapeutic Approaches.International journal of molecular sciences · 2022Review
- Autoimmunity, cancer and COVID-19 abnormally activate wound healing pathways: critical role of inflammation.Histochemistry and cell biology · 2022Review
- Cellular and Molecular Mechanism of Pulmonary Fibrosis Post-COVID-19: Focus on Galectin-1, -3, -8, -9.International journal of molecular sciences · 2022Review
- Daily Intraperitoneal Administration of Rosiglitazone Does Not Improve Lung Function or Alveolarization in Preterm Rabbits Exposed to Hyperoxia.Pharmaceutics · 2022Article
- Article
- Skin Fibrosis and Recovery Is Dependent on Wnt Activation via DPP4.The Journal of investigative dermatology · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
significanceOxygen, the main mode of support for premature infants with immature lungs, can cause toxicity by producing reactive oxygen species (ROS) that disrupt homeostasis; yet, these same molecules were entrained to promote vertebrate lung phylogeny. By providing a deeper understanding of this paradox, we propose physiologically rational strategies to prevent chronic lung disease (CLD) of prematurity. RECENT ADVANCES: To prevent neonatal hyperoxic lung damage biologically, we have exploited the alveolar defense mechanism(s) that evolutionarily evolved to combat increased atmospheric oxygen during the vertebrate water to land transition. CRITICAL ISSUES: Over the course of vertebrate lung evolution, ROS promoted the formation of lipofibroblasts, specialized adepithelial cells, which protect the alveoli against oxidant injury; peroxisome proliferator-activated receptor gamma (PPARγ), the master switch for lipofibroblast differentiation, prevents such oxidant lung injury, both by directly promoting mesodermal differentiation and its antioxidant defenses, and indirectly by stimulating the developmental epithelial-mesenchymal paracrine interactions that have physiologically determined lung surfactant production in accord with the lung's phylogenetic adaptation to atmospheric oxygen, preventing Respiratory Distress Syndrome at birth. FUTURE DIRECTIONS: The molecular strategy (PPARγ agonists) to prevent CLD of prematurity, proposed by us, although seems to be robust, effective, and safe under experimental conditions, it awaits detailed pharmacokinetic and pharmacodynamic studies for its safe and effective clinical translation to human infants. Antioxid. Redox Signal. 21, 1893-1904. "I have procured air [oxygen]…between five and six times as good as the best common air that I have ever met with." -Joseph Priestley, 1775.
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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.