4.5 Review

Particulate matter in COPD pathogenesis: an overview

Journal

INFLAMMATION RESEARCH
Volume 71, Issue 7-8, Pages 797-815

Publisher

SPRINGER BASEL AG
DOI: 10.1007/s00011-022-01594-y

Keywords

Chronic obstructive pulmonary disease; Particulate matter; Pathogenesis; Inflammation; Oxidative stress

Funding

  1. Department of Biotechnology, Ministry of Science and Technology, DBT-BUILDER [BT/INF/22/SP41295/2020]

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Chronic obstructive pulmonary disease (COPD) is a progressive lung disorder that burdens patients and is a leading cause of death worldwide. While cigarette smoke is recognized as the main causative factor, air pollution, particularly particulate matter (PM), has gained attention in recent years due to the increasing prevalence of COPD among non-smokers. Epidemiological studies have shown a strong correlation between airborne PM and COPD incidence and exacerbations. PM-induced oxidative stress is believed to play a major role in COPD inflammation, although the exact molecular mechanisms are still poorly understood. Mitochondrial dysfunction and autophagy have also emerged as important factors in COPD pathogenesis associated with oxidative stress. This review aims to understand the key molecular players in PM-mediated COPD pathogenesis by analyzing various experimental studies and epidemiological data, with the goal of identifying relevant preventive and therapeutic targets.
Chronic obstructive pulmonary disease (COPD) is a progressive lung disorder with substantial patient burden and leading cause of death globally. Cigarette smoke remains to be the most recognised causative factor behind COPD pathogenesis. Given the alarming increase in prevalence of COPD amongst non-smokers in recent past, a potential role of air pollution particularly particulate matter (PM) in COPD development has gained much attention of the scientists. Indeed, several epidemiological studies indicate strong correlation between airborne PM and COPD incidence/exacerbations. PM-induced oxidative stress seems to be the major player in orchestrating COPD inflammatory cycle but the exact molecular mechanism(s) behind such a process are still poorly understood. This may be due to the complexity of multiple molecular pathways involved. Oxidative stress-linked mitochondrial dysfunction and autophagy have also gained importance and have been the focus of recent studies regarding COPD pathogenesis. Accordingly, the present review is aimed at understanding the key molecular players behind PM-mediated COPD pathogenesis through analysis of various experimental studies supported by epidemiological data to identify relevant preventive/therapeutic targets in the area.

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