Mitochondrial dysfunction: a key player in the pathogenesis of cardiovascular diseases linked to air pollution

发病机制 钥匙(锁) 医学 环境卫生 生物 免疫学 生态学
作者
Sri Rahavi Boovarahan,Gino A. Kurian
出处
期刊:Reviews on environmental health [De Gruyter]
卷期号:33 (2): 111-122 被引量:50
标识
DOI:10.1515/reveh-2017-0025
摘要

Air pollution has become an environmental burden with regard to non-communicable diseases, particularly heart disease. It has been reported that air pollution can accelerate the development of heart failure and atrial fibrillation. Air pollutants encompass various particulate matters (PMs), which change the blood composition and heart rate and eventually leads to cardiac failure by triggering atherosclerotic plaque ruptures or by developing irreversible ischemia. A series of major epidemiological and observational studies have established the noxious effect of air pollutants on cardiovascular diseases (CVD), but the underlying molecular mechanisms of its susceptibility and the pathological disease events remain largely elusive and are predicted to be initiated in the cell organelle. The basis of this belief is that mitochondria are one of the major targets of environmental toxicants that can damage mitochondrial morphology, function and its DNA (manifested in non-communicable diseases). In this article, we review the literature related to air pollutants that adversely affect the progression of CVD and that target mitochondrial morphological and functional activities and how mitochondrial DNA (mtDNA) copy number variation, which reflects the airborne oxidant-induced cell damage, correlates with heart failure. We conclude that environmental health assessment should focus on the cellular/circulatory mitochondrial functional copy number status, which can predict the outcome of CVD.
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