ArticleJCI insight2018
AIBP augments cholesterol efflux from alveolar macrophages to surfactant and reduces acute lung inflammation.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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
39 citing papers in PubMed, 55 citations in OpenAlex.
- APOA1 binding protein promotes lymphatic cell fate and lymphangiogenesis by relieving caveolae-mediated inhibition of VEGFR3 signaling.Nature communications · 2025Article
- AIBP-LRP2-mediated HDL uptake restricts CXCR4Science advances · 2025Article
- ApoA1/HDL and sepsis-associated vascular endothelial injury: a narrative review.Critical care (London, England) · 2025Review
- Progressive Loss of Astrocytic AIBP Expression during Alzheimer's Disease Pathology.bioRxiv : the preprint server for biology · 2025Article
- Restoring AIBP expression in the retina provides neuroprotection in glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Alveolar macrophages: guardians of the alveolar lipid galaxy.Current opinion in lipidology · 2025Review
- Enhancement of Intracellular Cholesterol Efflux in Chondrocytes Leading to Alleviation of Osteoarthritis Progression.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- AIBP protects drug-induced liver injury by inhibiting MAPK-mediated NR4A1 expression.iScience · 2024Article
- AIBP Protects Müller Glial Cells Against Oxidative Stress-Induced Mitochondrial Dysfunction and Reduces Retinal Neuroinflammation.Antioxidants (Basel, Switzerland) · 2024Article
- AIBP controls TLR4 inflammarafts and mitochondrial dysfunction in a mouse model of Alzheimer's disease.Journal of neuroinflammation · 2024Article
- Mitigating Vascular Inflammation by Mimicking AIBP Mechanisms: A New Therapeutic End for Atherosclerotic Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Effect of apigetrin in pseudo-SARS-CoV-2-induced inflammatory and pulmonary fibrosis in vitro model.Scientific reports · 2024Article
- AIBP controls TLR4 inflammarafts and mitochondrial dysfunction in a mouse model of Alzheimer's disease.bioRxiv : the preprint server for biology · 2024Article
- Treatment Strategies for Anti-VEGF Resistance in Neovascular Age-Related Macular Degeneration by Targeting Arteriolar Choroidal Neovascularization.Biomolecules · 2024Review
- Review
- EGFR-driven lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth.Cancer discovery · 2024Article
- Article
- The Role of Pulmonary Surfactant Phospholipids in Fibrotic Lung Diseases.International journal of molecular sciences · 2022Review
- Article
- Reduced AIBP expression in bronchial epithelial cells of asthmatic patients: Potential therapeutic target.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Acute respiratory distress syndrome (ARDS) is characterized by an excessive pulmonary inflammatory response. Removal of excess cholesterol from the plasma membrane of inflammatory cells helps reduce their activation. The secreted apolipoprotein A-I binding protein (AIBP) has been shown to augment cholesterol efflux from endothelial cells to the plasma lipoprotein HDL. Here, we find that AIBP was expressed in inflammatory cells in the human lung and was secreted into the bronchoalveolar space in mice subjected to inhalation of LPS. AIBP bound surfactant protein B and increased cholesterol efflux from alveolar macrophages to calfactant, a therapeutic surfactant formulation. In vitro, AIBP in the presence of surfactant reduced LPS-induced p65, ERK1/2 and p38 phosphorylation, and IL-6 secretion by alveolar macrophages. In vivo, inhalation of AIBP significantly reduced LPS-induced airspace neutrophilia, alveolar capillary leak, and secretion of IL-6. These results suggest that, similar to HDL in plasma, surfactant serves as a cholesterol acceptor in the lung. Furthermore, lung injury increases pulmonary AIBP expression, which likely serves to promote cholesterol efflux to surfactant and reduce inflammation.
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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.