Ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structures
Fine particulate matter (PM2.5) is increasingly recognized for its detrimental effects on human health, with substantial evidence linking exposure to various forms of cell death and dysfunction across multiple organ systems. This review examines key cell death mechanisms triggered by PM2.5, includin...
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Elsevier
2025-01-01
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| Series: | Environment International |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0160412024007797 |
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| author | Yán Wāng |
| author_facet | Yán Wāng |
| author_sort | Yán Wāng |
| collection | DOAJ |
| description | Fine particulate matter (PM2.5) is increasingly recognized for its detrimental effects on human health, with substantial evidence linking exposure to various forms of cell death and dysfunction across multiple organ systems. This review examines key cell death mechanisms triggered by PM2.5, including PANoptosis, necroptosis, autophagy, and ferroptosis, while other forms such as oncosis, paraptosis, and cuprotosis remain unreported in relation to PM2.5 exposure. Mitochondria, endoplasmic reticulum, and lysosomes emerge as pivotal organelles in the disruption of cellular homeostasis, with mitochondrial dysfunction particularly implicated in metabolic dysregulation and the activation of pro-apoptotic pathways. Although PM2.5 primarily affects the nucleus, cytoskeleton, mitochondria, endoplasmic reticulum, and lysosomes, other organelles like ribosomes, Golgi apparatus, and peroxisomes have received limited attention. Interactions between these organelles, such as endoplasmic reticulum-associated mitochondrial membranes, lysosome-associated mitophagy, and mitochondria-nuclei retro-signaling may significantly contribute to the cytotoxic effects of PM2.5. The mechanisms of PM2.5 toxicity, encompassing oxidative stress, inflammatory responses, and metabolic imbalances, are described in detail. Notably, PM2.5 activates the NLRP3 inflammasome, amplifying inflammatory responses and contributing to chronic diseases. Furthermore, PM2.5 exposure disrupts genetic and epigenetic regulation, often resulting in cell cycle arrest and exacerbating cellular damage. The composition, concentration, and seasonal variability of PM2.5 modulate these effects, underscoring the complexity of PM2.5-induced cellular dysfunction. Despite significant advances in understanding these pathways, further research is required to elucidate the long-term effects of chronic PM2.5 exposure, the role of epigenetic regulation, and potential strategies to mitigate its harmful impact on human health. |
| format | Article |
| id | doaj-art-6523ba53ffd64d9c9d2f1a9161f7f5bc |
| institution | Kabale University |
| issn | 0160-4120 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
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| series | Environment International |
| spelling | doaj-art-6523ba53ffd64d9c9d2f1a9161f7f5bc2025-01-24T04:44:01ZengElsevierEnvironment International0160-41202025-01-01195109193Ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structuresYán Wāng0Address: Key Laboratory of Environmental Medicine Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, China.; Key Laboratory of Environmental Medicine Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu 210009, China; Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, Anhui 230032, ChinaFine particulate matter (PM2.5) is increasingly recognized for its detrimental effects on human health, with substantial evidence linking exposure to various forms of cell death and dysfunction across multiple organ systems. This review examines key cell death mechanisms triggered by PM2.5, including PANoptosis, necroptosis, autophagy, and ferroptosis, while other forms such as oncosis, paraptosis, and cuprotosis remain unreported in relation to PM2.5 exposure. Mitochondria, endoplasmic reticulum, and lysosomes emerge as pivotal organelles in the disruption of cellular homeostasis, with mitochondrial dysfunction particularly implicated in metabolic dysregulation and the activation of pro-apoptotic pathways. Although PM2.5 primarily affects the nucleus, cytoskeleton, mitochondria, endoplasmic reticulum, and lysosomes, other organelles like ribosomes, Golgi apparatus, and peroxisomes have received limited attention. Interactions between these organelles, such as endoplasmic reticulum-associated mitochondrial membranes, lysosome-associated mitophagy, and mitochondria-nuclei retro-signaling may significantly contribute to the cytotoxic effects of PM2.5. The mechanisms of PM2.5 toxicity, encompassing oxidative stress, inflammatory responses, and metabolic imbalances, are described in detail. Notably, PM2.5 activates the NLRP3 inflammasome, amplifying inflammatory responses and contributing to chronic diseases. Furthermore, PM2.5 exposure disrupts genetic and epigenetic regulation, often resulting in cell cycle arrest and exacerbating cellular damage. The composition, concentration, and seasonal variability of PM2.5 modulate these effects, underscoring the complexity of PM2.5-induced cellular dysfunction. Despite significant advances in understanding these pathways, further research is required to elucidate the long-term effects of chronic PM2.5 exposure, the role of epigenetic regulation, and potential strategies to mitigate its harmful impact on human health.http://www.sciencedirect.com/science/article/pii/S0160412024007797PM2.5PANoptosisFerroptosisEpigeneticsN6-methyladenosineCircular RNA |
| spellingShingle | Yán Wāng Ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structures Environment International PM2.5 PANoptosis Ferroptosis Epigenetics N6-methyladenosine Circular RNA |
| title | Ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structures |
| title_full | Ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structures |
| title_fullStr | Ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structures |
| title_full_unstemmed | Ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structures |
| title_short | Ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structures |
| title_sort | ambient fine particulate matter provokes multiple modalities of cell death via perturbation of subcellular structures |
| topic | PM2.5 PANoptosis Ferroptosis Epigenetics N6-methyladenosine Circular RNA |
| url | http://www.sciencedirect.com/science/article/pii/S0160412024007797 |
| work_keys_str_mv | AT yanwang ambientfineparticulatematterprovokesmultiplemodalitiesofcelldeathviaperturbationofsubcellularstructures |