ArticleAmerican journal of respiratory and critical care medicine2010
Apolipoprotein E negatively regulates house dust mite-induced asthma via a low-density lipoprotein receptor-mediated pathway.
Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 107 citations in OpenAlex.
- The very low density lipoprotein receptor attenuates house dust mite-induced airway inflammation by suppressing dendritic cell-mediated adaptive immune responses.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Dupilumab Dampens Mucosal Type 2 Response During Acetylsalicylic Acid Challenge in N-ERD Patients.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026Article
- Repurposing lipid-lowering drugs on asthma and lung function: evidence from a genetic association analysis.Journal of translational medicine · 2024Article
- Association between serum lipid and all-cause mortality in asthmatic populations: a cohort study.Lipids in health and disease · 2024Article
- Genetic association of inflammatory marker GlycA with lung function and respiratory diseases.Nature communications · 2024Article
- Article
- Airway fibrin formation cascade in allergic asthma exacerbation: implications for inflammation and remodeling.Clinical proteomics · 2022Article
- PRMT5 in T Cells Drives Th17 Responses, Mixed Granulocytic Inflammation, and Severe Allergic Airway Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Melatonin Suppresses Macrophage M1 Polarization and ROS-Mediated Pyroptosis via Activating ApoE/LDLR Pathway in Influenza A-Induced Acute Lung Injury.Oxidative medicine and cellular longevity · 2022Article
- Chronic Allergen Challenge Induces Corticosteroid Insensitivity With Persistent Airway Remodeling and Type 2 Inflammation.Frontiers in pharmacology · 2022Article
- Comprehensive Analysis of Nasal Polyps Reveals a More Pronounced Type 2 Transcriptomic Profile of Epithelial Cells and Mast Cells in Aspirin-Exacerbated Respiratory Disease.Frontiers in immunology · 2022Article
- Update in Adult Asthma 2020.American journal of respiratory and critical care medicine · 2021Review
- Scavenger Receptor BI Attenuates IL-17A-Dependent Neutrophilic Inflammation in Asthma.American journal of respiratory cell and molecular biology · 2021Article
- The Long and Winding Road from GWAS to Obstructive Lung Disease: Is There a Role for LRP1?American journal of respiratory cell and molecular biology · 2021Article
- Apolipoprotein E Signals via TLR4 to Induce CXCL5 Secretion by Asthmatic Airway Epithelial Cells.American journal of respiratory cell and molecular biology · 2020Article
- Article
- Apolipoprotein E is a concentration-dependent pulmonary danger signal that activates the NLRP3 inflammasome and IL-1β secretion by bronchoalveolar fluid macrophages from asthmatic subjects.The Journal of allergy and clinical immunology · 2019Article
- Abnormal composition and function of high-density lipoproteins in atopic dermatitis patients.Allergy · 2019Article
- Pilot-Scale Study Of Human Plasma Proteomics Identifies ApoE And IL33 As Markers In Atopic Asthma.Journal of asthma and allergy · 2019Article
- Low-density lipoprotein receptor-related protein 1 attenuates house dust mite-induced eosinophilic airway inflammation by suppressing dendritic cell-mediated adaptive immune responses.The Journal of allergy and clinical immunology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
Abstract
rationaleDistinct sets of corticosteroid-unresponsive genes modulate disease severity in asthma.
objectivesTo identify corticosteroid-unresponsive genes that provide new insights into disease pathogenesis and asthma therapeutics.
methodsExperimental murine asthma was induced by nasal administration of house dust mite for 5 days per week. Dexamethasone and apolipoprotein E (apo E) mimetic peptides were administered via osmotic minipumps. MEASUREMENTS AND MAIN
resultsGenome-wide expression profiling of the lung transcriptome in a house dust mite-induced model of murine asthma identified increases in apo E mRNA levels that persisted despite corticosteroid treatment. House dust mite-challenged apo E⁻(/)⁻ mice displayed enhanced airway hyperreactivity and goblet cell hyperplasia, which could be rescued by administration of an apo E(130-149) mimetic peptide. Administration of the apo E(130-149) mimetic peptide to house dust mite-challenged apo E⁻(/)⁻ mice also inhibited eosinophilic airway inflammation, IgE production, and the expression of Th2 and Th17 cytokines. House dust mite-challenged low-density lipoprotein receptor (LDLR) knockout mice displayed a similar phenotype as apo E⁻(/)⁻ mice with enhanced airway hyperreactivity, goblet cell hyperplasia, and mucin gene expression, but could not be rescued by the apo E(130-149) mimetic peptide, consistent with a LDLR-dependent mechanism.
conclusionsThese findings for the first time identify an apo E-LDLR pathway as an endogenous negative regulator of airway hyperreactivity and goblet cell hyperplasia in asthma. Furthermore, our results demonstrate that strategies that activate the apo E-LDLR pathway, such as apo E mimetic peptides, might be developed into a novel treatment approach for patients with asthma.
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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.