Department of Biochemistry, Panjab University, Chandigarh, 160014, India.
University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, 160014, India.
Inflamm Res. 2022 Aug;71(7-8):797-815. doi: 10.1007/s00011-022-01594-y. Epub 2022 Jun 16.
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.
慢性阻塞性肺疾病(COPD)是一种具有重大患者负担的进行性肺部疾病,也是全球主要的死亡原因。吸烟仍然是 COPD 发病机制中最被认可的致病因素。鉴于近年来非吸烟者中 COPD 的患病率惊人增加,空气污染特别是颗粒物(PM)在 COPD 发展中的潜在作用引起了科学家们的极大关注。事实上,几项流行病学研究表明,空气中的 PM 与 COPD 的发病率/加重之间存在很强的相关性。PM 引起的氧化应激似乎是 COPD 炎症循环的主要参与者,但这种过程的确切分子机制仍知之甚少。这可能是由于涉及的多个分子途径的复杂性所致。氧化应激相关的线粒体功能障碍和自噬也变得重要起来,并成为最近关于 COPD 发病机制的研究重点。因此,本综述旨在通过分析流行病学数据支持的各种实验研究,了解 PM 介导的 COPD 发病机制背后的关键分子参与者,以确定该领域的相关预防/治疗靶点。