ArticleAmerican journal of respiratory cell and molecular biology2019
Impairment of Fatty Acid Oxidation in Alveolar Epithelial Cells Mediates Acute Lung Injury.
Article in American journal of respiratory cell and molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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59 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 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
- Article
- Protective role of fatty acid oxidation against epithelial barrier dysfunction in allergic asthma.Redox report : communications in free radical research · 2026Article
- Fuelling repair: metabolic regulation of alveolar type 2 cell fate in lung regeneration and disease.Disease models & mechanisms · 2026Review
- A multifunctional ICAM1-directed MnO₂@ZIF8 nanoplatform with Tanshinone IIA synergistically reverses senescence and restores alveolar regeneration in septic lung injury.Journal of nanobiotechnology · 2026Article
- Baihe Gujin decoction ameliorates sepsis-induced acute lung injury through Nrf2/GPX4-mediated antioxidant defense and PPARα-driven metabolic reprogramming: a multi-omics investigation.Frontiers in immunology · 2026Article
- Mitochondrial programmed cell death in bronchopulmonary dysplasia: mechanisms and therapeutic targets.Frontiers in physiology · 2026Review
- Inhalation & intravenous: umbilical cord mesenchymal stem cell-derived exosomes therapy strategy for acute respiratory distress syndrome in a murine model.Journal of thoracic disease · 2025Article
- Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025Review
- Advances in natural product-based nanoparticles for the treatment of acute lung injury.Materials today. Bio · 2025Review
- Dimethyl fumarate alleviates inflammation during high altitude hypoxia induced acute lung injury by upregulating Nrf2/SLC7A11 pathway in ferroptosis.Clinical proteomics · 2025Article
- Are alveolar type 2 cells "oversaturated" in obesity and ARDS?American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Alveolar Epithelial Cell Dysfunction in Acute Respiratory Distress Syndrome: Mechanistic Insights and Targeted Interventions.Biomedicines · 2025Review
- 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
- Idiopathic Pulmonary Fibrosis Caused by Damaged Mitochondria and Imbalanced Protein Homeostasis in Alveolar Epithelial Type II Cell.Advanced biology · 2025Review
- Vitexin mitigates oxidative stress, mitochondrial damage, pyroptosis and regulates small nucleolar RNA host gene 1/DNA methyltransferase 1/microRNA-495 axis in sepsis-associated acute lung injury.Inflammopharmacology · 2025Article
- Bioactive Nanomaterials: Comprehensive Monitoring and Regulation of Acute Pancreatitis Induced Acute Lung Injury.International journal of nanomedicine · 2025Review
- Peroxisome Metabolism Pathway and EHHADH Expression are Downregulated in Macrophages in Neutrophilic Asthma.Allergy, asthma & immunology research · 2025Article
- A crucial role of the malate aspartate shuttle in metabolic reprogramming in TNF-induced SIRS.Frontiers in immunology · 2025Article
- Lung contusion complicated by pneumonia worsens lung injury via the inflammatory effect of alveolar small extracellular vesicles on macrophages and epithelial cells.The journal of trauma and acute care surgery · 2025Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Profound impairment in cellular oxygen consumption, referred to as cytopathic dysoxia, is one of the pathological hallmarks in the lungs of patients with pathogen-induced acute lung injury (ALI). However, the underlying mechanism for this functional defect remains largely unexplored. In this study, we found that primary mouse alveolar epithelial cells (AECs) conducted robust fatty acid oxidation (FAO). More importantly, FAO was strikingly impaired in AECs of mice with LPS-induced ALI. The metabolic deficiency in these cells was likely due to decreased expression of key mediators involved in FAO and mitochondrial bioenergenesis, such as peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, carnitine palmitoyltransferase 1A, and medium-chain acyl-CoA dehydrogenase (CAD). We found that treatment of alveolar epithelial line MLE-12 cells with BAL fluids from mice with ALI decreased FAO, and this effect was largely replicated in MLE-12 cells treated with the proinflammatory cytokine TNF-α, which was consistent with downregulations of PGC-1α, carnitine palmitoyltransferase 1A, long-chain CAD, and medium-chain CAD in the same treated cells. Furthermore, we found that the BAL fluids from ALI mice and TNF-α inhibited MLE-12 bioenergenesis and promoted cell apoptosis. In delineation of the role of FAO in ALI in vivo, we found that conditional ablation of AEC PGC-1α aggravated LPS-induced ALI. In contrast, fenofibrate, an activator of the PPAR-α/PGC-1α cascade, protected mice from this pathology. In summary, these data suggest that FAO is essential to AEC bioenergenesis and functional homeostasis. This study also indicates that FAO impairment-induced AEC dysfunction is an important contributing factor to the pathogenesis of ALI.
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Registered trials
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