ReviewOxidative medicine and cellular longevity2013
Nrf2 is a protective factor against oxidative stresses induced by diesel exhaust particle in allergic asthma.
Review in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Recent understanding of immunometabolic remodeling in pulmonary macrophages: homeostasis, chronic respiratory diseases, and therapeutic targeting.Frontiers in pharmacology · 2026Review
- Impact of Continuously Improved Air Quality on Mental Health: A Quasi-experimental Study Based on Longitudinal Observations for Chinese Adults.Environment & health (Washington, D.C.) · 2025Article
- Exploring Nrf2 as a Potential Biomarker in Asthma: Links to Hypoxia, Oxidative Stress, and Ferroptosis in a Cross-Sectional Study.Journal of asthma and allergy · 2025Article
- Article
- NRF2-Dependent Placental Effects Vary by Sex and Dose following Gestational Exposure to Ultrafine Particles.Antioxidants (Basel, Switzerland) · 2022Article
- NRF2 Protects against Altered Pulmonary T Cell Differentiation in Neonates Following In Utero Ultrafine Particulate Matter Exposure.Antioxidants (Basel, Switzerland) · 2022Article
- Melatonin antagonizes ozone-exacerbated asthma by inhibiting the TRPV1 channel and stabilizing the Nrf2 pathway.Environmental science and pollution research international · 2021Article
- Article
- Environmental exposures and mechanisms in allergy and asthma development.The Journal of clinical investigation · 2019Review
- In utero ultrafine particulate matter exposure causes offspring pulmonary immunosuppression.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Resveratrol protects against oxidative stress by activating the Keap-1/Nrf2 antioxidant defense system in obese-asthmatic rats.Experimental and therapeutic medicine · 2018Article
- Furanodienone induces G0/G1 arrest and causes apoptosis via the ROS/MAPKs-mediated caspase-dependent pathway in human colorectal cancer cells: a study in vitro and in vivo.Cell death & disease · 2017Article
- Diesel exhaust alters the response of cultured primary bronchial epithelial cells from patients with chronic obstructive pulmonary disease (COPD) to non-typeable Haemophilus influenzae.Respiratory research · 2017Article
- Phloretin Attenuates Allergic Airway Inflammation and Oxidative Stress in Asthmatic Mice.Frontiers in immunology · 2017Article
- Air pollution and allergic diseases.Current opinion in pediatrics · 2015Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological studies have shown that air pollutants, such as diesel exhaust particle (DEP), are implicated in the increased incidence of allergic airway disorders. In vitro studies of molecular mechanisms have focused on the role of reactive oxygen species generated directly and indirectly by the exposure to DEP. Antioxidants effectively reduce the allergic inflammatory effects induced by DEP both in vitro and in vivo. On the other hand, Nrf2 is a transcription factor essential for the inducible and/or constitutive expression of phase II and antioxidant enzymes. Disruption of Nrf2 enhances susceptibility to airway inflammatory responses and exacerbation of allergic inflammation induced by DEP in mice. Host responses to DEP are regulated by a balance between antioxidants and proinflammatory responses. Nrf2 may be an important protective factor against oxidative stresses induced by DEP in airway inflammation and allergic asthma and is expected to contribute to chemoprevention against DEP health effects in susceptible individuals.
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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.