ArticleJournal of hazardous materials2023
Genetic deletion or pharmacological inhibition of soluble epoxide hydrolase attenuated particulate matter 2.5 exposure mediated lung injury.
Article in Journal of hazardous materials, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 41 citations in OpenAlex.
- Uhrf1-Mediated PKM2 Degradation via Ubiquitination Alleviates Inflammation and Pyroptosis in Inflammatory Bowel Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting eEF1A1 With Baicalein to Block eEF1A1/Prdx4 Interaction for Treating Sepsis-Mediated Lung Injury.Exploration (Beijing, China) · 2026Article
- Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026Review
- Article
- [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
- Targeted soluble epoxide hydrolase inhibits M1 macrophage polarization to improve cartilage injury in temporomandibular joint osteoarthritis.Journal of translational medicine · 2025Article
- Targeting PBK with small-molecule 1-Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- PM2.5 Induces Cell-Specific Transcriptomic Alterations in the Lungs of Juvenile Mice.Journal of inflammation research · 2025Article
- Inhibition of soluble epoxide hydrolase in endotoxin induced pig lung injury.Frontiers in pharmacology · 2025Article
- Green Tea Attenuates the Particulate Matter (PM)Journal of microbiology and biotechnology · 2024Article
- Polyphenols of the Inuleae-Inulinae and Their Biological Activities: A Review.Molecules (Basel, Switzerland) · 2024Review
- Attenuation of Polycyclic Aromatic Hydrocarbon (PAH)-Induced Carcinogenesis and Tumorigenesis by Omega-3 Fatty Acids in Mice In Vivo.International journal of molecular sciences · 2024Article
- Inhaled toxicants and pulmonary lipid metabolism: biological consequences and therapeutic interventions.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- IκB kinase β (IKKβ): Structure, transduction mechanism, biological function, and discovery of its inhibitors.International journal of biological sciences · 2023Review
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Air pollution represented by particulate matter 2.5 (PM2.5) is closely related to diseases of the respiratory system. Although the understanding of its mechanism is limited, pulmonary inflammation is closely correlated with PM2.5-mediated lung injury. Soluble epoxide hydrolase (sEH) and epoxy fatty acids play a vital role in the inflammation. Herein, we attempted to use the metabolomics of oxidized lipids for analyzing the relationship of oxylipins with lung injury in a PM2.5-mediated mouse model, and found that the cytochrome P450 oxidases/sEH mediated metabolic pathway was involved in lung injury. Furthermore, the sEH overexpression was revealed in lung injury mice. Interestingly, sEH genetic deletion or the selective sEH inhibitor TPPU increased levels of epoxyeicosatrienoic acids (EETs) in lung injury mice, and inactivated pulmonary macrophages based on the MAPK/NF-κB pathway, resulting in protection against PM2.5-mediated lung injury. Additionally, a natural sEH inhibitor luteolin from Inula japonica displayed a pulmonary protective effect towards lung injury mediated by PM2.5 as well. Our results are consistent with the sEH message and protein being both a marker and mechanism for PM2.5-induced inflammation, which suggest its potential as a pharmaceutical target for treating diseases of the respiratory system.
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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.