Volume 1, Issue 4 (9-2025)
2025, 1(4): 20-26 |
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kheiry M, Maleki F. The Role of Air Pollution in Inducing Ferroptosis: Mechanisms, Evidence, and Innovative Perspectives: Review Article. Journal of Health Sciences Perspective 2025; 1 (4) :20-26
URL: http://jhsp.medilam.ac.ir/article-1-45-en.html
URL: http://jhsp.medilam.ac.ir/article-1-45-en.html
Clinical Research Development Unit, Shahid Mostafa Khomeini Hospital, Ilam University of medical Sciences, Ilam, Iran, ORCID: 0000-0001-8887-8368
Abstract: (37 Views)
Introduction: Air pollution is a complex environmental hazard composed of particulate matter (PM₂.₅, PM₁₀), heavy metals, ozone, nitrogen dioxide, and polycyclic aromatic hydrocarbons. These pollutants are strongly associated with respiratory, cardiovascular, and neurological disorders. At the molecular level, pollutants induce oxidative stress, inflammation, and mitochondrial dysfunction. Ferroptosis, an iron-dependent regulated cell death characterized by lipid peroxidation and glutathione depletion, has recently emerged as a critical pathway in pollution-related cellular injury. This review aims to summarize the mechanistic links between air pollution and ferroptosis, highlight supporting experimental and clinical evidence, and discuss future therapeutic perspectives.
Materials & Methods: A systematic literature review was conducted in PubMed, Scopus, and Web of Science databases using the keywords ferroptosis, air pollution, and mechanisms. Articles were screened and analyzed following PRISMA guidelines. Both in vitro, in vivo, and limited human studies were evaluated. Statistical synthesis was descriptive, as data heterogeneity precluded quantitative meta-analysis.
Results: Findings from multiple studies demonstrate that pollutants induce ferroptosis through iron overload, suppression of the cystine/glutamate antiporter (system Xc⁻), inactivation of glutathione peroxidase 4 (GPX4), and excessive reactive oxygen species production. Markers of ferroptosis, including increased lipid peroxidation and reduced GPX4, were consistently observed. Evidence links ferroptosis to pollutant-induced chronic diseases such as chronic obstructive pulmonary disease (COPD), cardiovascular dysfunction, and neurodegenerative disorders.
Conclusion: Ferroptosis represents a mechanistic bridge between air pollution and chronic disease development. Beyond oxidative stress, it acts as a pathological orchestrator driving inflammation and tissue remodeling. Targeting ferroptosis offers innovative therapeutic opportunities to mitigate the global health impacts of air pollution.
Materials & Methods: A systematic literature review was conducted in PubMed, Scopus, and Web of Science databases using the keywords ferroptosis, air pollution, and mechanisms. Articles were screened and analyzed following PRISMA guidelines. Both in vitro, in vivo, and limited human studies were evaluated. Statistical synthesis was descriptive, as data heterogeneity precluded quantitative meta-analysis.
Results: Findings from multiple studies demonstrate that pollutants induce ferroptosis through iron overload, suppression of the cystine/glutamate antiporter (system Xc⁻), inactivation of glutathione peroxidase 4 (GPX4), and excessive reactive oxygen species production. Markers of ferroptosis, including increased lipid peroxidation and reduced GPX4, were consistently observed. Evidence links ferroptosis to pollutant-induced chronic diseases such as chronic obstructive pulmonary disease (COPD), cardiovascular dysfunction, and neurodegenerative disorders.
Conclusion: Ferroptosis represents a mechanistic bridge between air pollution and chronic disease development. Beyond oxidative stress, it acts as a pathological orchestrator driving inflammation and tissue remodeling. Targeting ferroptosis offers innovative therapeutic opportunities to mitigate the global health impacts of air pollution.
Type of Study: Research |
Subject:
Air Pollution
Received: 2025/07/9 | Accepted: 2025/08/29 | Published: 2025/09/22
Received: 2025/07/9 | Accepted: 2025/08/29 | Published: 2025/09/22
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