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자료유형
학술저널
저자정보
홍주혁 (강원대학교) 양세란 (강원대학교)
저널정보
강원대학교 환경연구소 Journal of the Environment Journal of the Environment Vol.17 No.2
발행연도
2024.12
수록면
47 - 69 (23page)

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Although chronic obstructive pulmonary disease (COPD) has traditionally been associated with smoking, recent evidence suggests that particulate matter (PM) exposure is emerging as a significant risk factor, particularly in non-smokers. This review examines the intricate relationship between PM exposure, neutrophil extracellular traps (NETs), and COPD pathogenesis, with a particular focus on the molecular mechanisms underlying NETosis in PM-induced COPD. PM, especially fine (PM<sub>2.5</sub>) and ultrafine particles, can penetrate deep into the airways, triggering various inflammatory responses. Among these responses, NETosis, a unique form of neutrophil cell death characterized by the release of DNA and antimicrobial proteins, has gained attention as a crucial mechanism in COPD pathophysiology. Recent studies have demonstrated that over 90% of exacerbated COPD patients show evidence of NET formation, compared to 45% in stable COPD patients, suggesting a strong correlation between NET formation and disease severity. The molecular mechanisms of NETosis involve complex processes including chromatin decondensation through PAD4-mediated histone citrullination, nuclear membrane breakdown via lamin degradation, and cytoskeletal reorganization, PM exposure can trigger these processes through various pathways, particularly through the generation of reactive oxygen species (ROS) and the activation of inflammatory signaling cascades. In COPD, NETs contribute to disease progression by increasing mucus viscosity, activating NLRP3 inflammasomes, and inducing CXCL8 release, thereby perpetuating inflammation. This review synthesizes current knowledge about the role of NETs in PMinduced COPD while addressing critical questions regarding the NET formation, specific triggers in COPD patients, and potential therapeutic strategies targeting NETs. Understanding these mechanisms may pave the way for novel therapeutic approaches for preventing and treating PM-induced COPD.

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Abstract
서론
미세먼지와 만성폐쇄성폐질환
PM과 면역세포
호중구활성
결론
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