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Licensed Unlicensed Requires Authentication Published by De Gruyter January 18, 2018

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

  • Sri Rahavi Boovarahan and Gino A. Kurian EMAIL logo

Abstract

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.


Corresponding author: Gino A. Kurian, Senior Assistant Professor, Vascular Biology Laboratory, School of Chemical and Biotechnology, SASTRA University, Thanjavur, Tamilnadu 613401, India, Phone: +919047965425, Fax: +914362-264120, E-mail:

Acknowledgments

We thank the Vice-Chancellor, SASTRA University, for the infrastructure facility and Kausthubh R for his assistance in the manuscript preparation.

  1. Author Statement

  2. Research funding: This study was supported by the Indian Council of Medical Research, New Delhi (5/4/1-14/12-NCD-II). Conflict of interest: Authors state no conflict of interest. Informed consent: Informed consent is not applicable. Ethical approval: The conducted research is not related to either human or animal use.

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Received: 2017-08-09
Accepted: 2017-12-11
Published Online: 2018-01-18
Published in Print: 2018-06-27

©2018 Walter de Gruyter GmbH, Berlin/Boston

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