ArticleThe Journal of biological chemistry2014
Long-chain acyl-CoA dehydrogenase deficiency as a cause of pulmonary surfactant dysfunction.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- The role of fatty acid metabolism in acute lung injury: a special focus on immunometabolism.Cellular and molecular life sciences : CMLS · 2024Pooled it
- Human genetic variants and age are the strongest predictors of humoral immune responses to common pathogens and vaccines.Genome medicine · 2018Trial
- High-fat diet obesity exacerbates acute lung injury-induced dysregulation of fatty acid oxidation in alveolar epithelial type 2 cells.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Article
- Alveolar epithelial cells mitigate neutrophilic inflammation in lung injury through regulating mitochondrial fatty acid oxidation.Nature communications · 2024Article
- Structural basis for expanded substrate specificities of human long chain acyl-CoA dehydrogenase and related acyl-CoA dehydrogenases.Scientific reports · 2024Article
- A review of fatty acid oxidation disorder mouse models.Molecular genetics and metabolism · 2024Review
- Structural Basis for Expanded Substrate SpeciResearch square · 2024Article
- The Physiological and Pathological Role of Acyl-CoA Oxidation.International journal of molecular sciences · 2023Review
- Serum metabolomic signatures of fatty acid oxidation defects differentiate host-response subphenotypes of acute respiratory distress syndrome.Respiratory research · 2023Article
- ITCH deficiency clinical phenotype expansion and mitochondrial dysfunction.Molecular genetics and metabolism reports · 2022Article
- Progressive Metabolic Abnormalities Associated with the Development of Neonatal Bronchopulmonary Dysplasia.Nutrients · 2022Article
- The oncogenic landscape of the idiopathic pulmonary fibrosis: a narrative review.Translational lung cancer research · 2022Review
- Mitochondrial dysfunction associated with TANGO2 deficiency.Scientific reports · 2022Article
- A "Weird" Mitochondrial Fatty Acid Oxidation as a Metabolic "Secret" of Cancer.Oxidative medicine and cellular longevity · 2022Review
- Pervasive inflammatory activation in patients with deficiency in very-long-chain acyl-coA dehydrogenase (VLCADD).Clinical & translational immunology · 2021Article
- Identification of common signatures in idiopathic pulmonary fibrosis and lung cancer using gene expression modeling.BMC cancer · 2020Article
- Alveolar lipids in pulmonary disease. A review.Lipids in health and disease · 2020Review
- An acyl-CoA dehydrogenase microplate activity assay using recombinant porcine electron transfer flavoprotein.Analytical biochemistry · 2019Article
- The fatty acid oxidation enzyme long-chain acyl-CoA dehydrogenase can be a source of mitochondrial hydrogen peroxide.Redox biology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 5 institutions in 1 country.
Funding
Abstract
Long-chain acyl-CoA dehydrogenase (LCAD) is a mitochondrial fatty acid oxidation enzyme whose expression in humans is low or absent in organs known to utilize fatty acids for energy such as heart, muscle, and liver. This study demonstrates localization of LCAD to human alveolar type II pneumocytes, which synthesize and secrete pulmonary surfactant. The physiological role of LCAD and the fatty acid oxidation pathway in lung was subsequently studied using LCAD knock-out mice. Lung fatty acid oxidation was reduced in LCAD(-/-) mice. LCAD(-/-) mice demonstrated reduced pulmonary compliance, but histological examination of lung tissue revealed no obvious signs of inflammation or pathology. The changes in lung mechanics were found to be due to pulmonary surfactant dysfunction. Large aggregate surfactant isolated from LCAD(-/-) mouse lavage fluid had significantly reduced phospholipid content as well as alterations in the acyl chain composition of phosphatidylcholine and phosphatidylglycerol. LCAD(-/-) surfactant demonstrated functional abnormalities when subjected to dynamic compression-expansion cycling on a constrained drop surfactometer. Serum albumin, which has been shown to degrade and inactivate pulmonary surfactant, was significantly increased in LCAD(-/-) lavage fluid, suggesting increased epithelial permeability. Finally, we identified two cases of sudden unexplained infant death where no lung LCAD antigen was detectable. Both infants were homozygous for an amino acid changing polymorphism (K333Q). These findings for the first time identify the fatty acid oxidation pathway and LCAD in particular as factors contributing to the pathophysiology of pulmonary disease.
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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.