ArticleAnnals of translational medicine2020
Fine particulate matter exposure promotes M2 macrophage polarization through inhibiting histone deacetylase 2 in the pathogenesis of chronic obstructive pulmonary disease.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- A new mouse model of biomass smoke-related chronic obstructive pulmonary disease combining porcine pancreatic elastase nebulization.Journal of thoracic disease · 2025Article
- Increased HLA-DR Expression on M2a Monocytes and Helper T Cells in Patients with COPD and Asthma-COPD Overlap Contributes to Disease Severity via Apoptosis and ROS.Antioxidants (Basel, Switzerland) · 2025Article
- Renal transcriptome-wide analyses in association with kidney black carbon load.Particle and fibre toxicology · 2025Article
- [PM2.5-induced M2 Polarization and IL-1α Secretion by Tumor-associated Macrophages Promotes Lung Adenocarcinoma Progression].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Article
- Unraveling the mechanisms underlying air pollution-induced dysfunction of the oral-gut-brain axis: implications for human health and well-being.Asian biomedicine : research, reviews and news · 2025Review
- Particulate matter-induced epigenetic modifications and lung complications.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Molecular changes underlying pulmonary emphysema and chronic bronchitis in Chronic Obstructive Pulmonary Disease: An updated review.Histology and histopathology · 2024Review
- A study of inflammatory biomarkers in crystalline silica exposed rock drillers.International archives of occupational and environmental health · 2024Article
- Macrophage Polarization and Functions in Pathogenesis of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2024Review
- Deflamin Attenuated Lung Tissue Damage in an Ozone-Induced COPD Murine Model by Regulating MMP-9 Catalytic Activity.International journal of molecular sciences · 2024Article
- Article
- Unlocking Macrophage Secrets: Histone Deacetylases in Chronic Transplant Rejection.Results and problems in cell differentiation · 2024Review
- On the path to predicting immune responses in the lung: Modeling the pulmonary innate immune system at the air-liquid interface (ALI).European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2023Review
- BMAL1/p53 mediating bronchial epithelial cell autophagy contributes to PM2.5-aggravated asthma.Cell communication and signaling : CCS · 2023Article
- Exposure duration of ambient fine particulate matter determines the polarization of macrophages.Central-European journal of immunology · 2023Article
- Review
- Inflammation resolution in environmental pulmonary health and morbidity.Toxicology and applied pharmacology · 2022Review
- Single-cell transcriptomics reveals immune dysregulation mediated by IL-17A in initiation of chronic lung injuries upon real-ambient particulate matter exposure.Particle and fibre toxicology · 2022Article
- Recent Insights into Particulate Matter (PMInternational journal of environmental research and public health · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality globally. Fine particulate matter (PM2.5) has been indicated to be a major detrimental risk factor for COPD by numerous epidemiological studies. Histone deacetylase 2 (HDAC2), a critical regulator of chromatin remodeling, plays a pivotal role in the development of COPD. However, the underlying mechanisms regarding the relationship between PM2.5 and HDAC2 in the pathogenesis of COPD have yet to be elucidated. In the present study, we aim to investigate the role and the underlying mechanism of HDAC2 in the development of PM2.5-induced COPD.
methodsThe effects of PM2.5 exposure on M2 macrophage polarization and the expression levels of HDAC2 were examined
resultsPM2.5 exposure down-regulated the protein level of HDAC2 and enhanced M2 macrophage polarization
conclusionsPM2.5 facilitated M2 polarization by inhibiting HDAC2, leading to the development of COPD. Targeting of HDAC2 would provide a novel approach to prevent the development of PM2.5 exposure-induced COPD.
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