ArticleClinical and translational medicine2020
PI3K inhibitor treatment ameliorates the glucocorticoid insensitivity of PBMCs in severe asthma.
Article in Clinical and translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Cross-Talk Between Histamine HPharmacology research & perspectives · 2026Article
- Lp-PLA2-derived LysoPC drives dendritic cell immunogenic activation and Th17 inflammation in severe asthma.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Multifaceted mechanistic exploration ofFrontiers in cell and developmental biology · 2026Article
- Precision identification and targeted therapy for neutrophilic asthma: from molecular mechanisms to clinical translation.Frontiers in immunology · 2026Review
- PI3K pathway activation in severe asthma is linked to steroid insensitivity and adverse outcomes.The journal of allergy and clinical immunology. Global · 2025Article
- Intranasal dupilumab improves responsiveness to steroid in an asthma mouse model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Integrating Extracellular Vesicles Proteomics and Clinical Parameters to Develop a High-Precision Predictive Model for Severe Asthma.Journal of inflammation research · 2025Article
- Application of Biologics in the Treatment of Asthma in the Past Two Decades: A Bibliometric Analysis and Beyond.Journal of asthma and allergy · 2025Review
- Oxidative Stress and Antioxidants in Pediatric Asthma's Evolution and Management.Antioxidants (Basel, Switzerland) · 2024Review
- Transcriptional profiles of peripheral eosinophils in chronic obstructive pulmonary disease and asthma-An exploratory study.Journal of cellular and molecular medicine · 2024Article
- Effect of allyl isothiocyanate on 4-HNE induced glucocorticoid resistance in COPD and the underlying mechanism.Heliyon · 2024Article
- GRespiratory research · 2024Review
- PP121, a dual inhibitor of tyrosine and phosphoinositide kinases, relieves airway hyperresponsiveness, mucus hypersecretion and inflammation in a murine asthma model.Molecular medicine (Cambridge, Mass.) · 2023Article
- Emerging roles and therapeutic implications of HDAC2 and IL-17A in steroid-resistant asthma.Chinese medical journal pulmonary and critical care medicine · 2023Review
- Article
- Oxidative Stress, Environmental Pollution, and Lifestyle as Determinants of Asthma in Children.Biology · 2023Review
- Peripheral neutrophils and oxidative stress-associated molecules for predicting the severity of asthma: a cross-sectional study based on multidimensional assessment.Frontiers in medicine · 2023Article
- CC16 as an Inflammatory Biomarker in Induced Sputum Reflects Chronic Obstructive Pulmonary Disease (COPD) Severity.International journal of chronic obstructive pulmonary disease · 2023Article
- Insights into potential mechanisms of asthma patients with COVID-19: A study based on the gene expression profiling of bronchoalveolar lavage fluid.Computers in biology and medicine · 2022Article
- Targeting the PI3K/Akt/mTOR pathway: A therapeutic strategy in COVID-19 patients.Immunology letters · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundGlucocorticoid (GC) insensitivity is an important feature of severe and fatal asthma. Oxidative stress can induce phosphoinositide-3-kinase (PI3K) activation, contributing to the development of GC insensitivity in chronic airway diseases. However, the underlying molecular mechanism of PI3K in the pathogenesis of severe asthma remains unknown.
methodsWe isolated peripheral blood mononuclear cells (PBMCs) from 34 participants (12 patients with mild/moderate asthma, 10 patients with severe asthma, and 12 control subjects). H
resultsPBMCs from patients with severe asthma exhibited dose-dependent and time-dependent GC insensitivity, which correlated with reduced activity of histone deacetylase 2 (HDAC2) (p < 0.05) and elevated expression of proinflammatory genes [nuclear factor-κB (NF-κB) and activator protein-1 (AP-1)] (p < 0.01) compared with these parameters in the control group. The PI3K inhibitors (BZE235 and LY294002) significantly restored the GC sensitivity of PBMCs from patients with severe asthma. In vitro, the PI3K inhibitors (BZE235 and LY294002) ameliorated GC insensitivity in H
conclusionsThis study demonstrates that PI3K inhibitors ameliorate GC insensitivity in severe asthma by restoring HDAC2 activity and inhibiting the phosphorylation of nuclear signaling transcription factors.
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