Mitochondria and traffic-related air pollution linked coronary artery calcification: exploring the missing link

The continuing increase in the exposure to Traffic-related air pollution (TRAP) in the general population is predicted to result in a higher incidence of non-communicable diseases like cardiovascular disease. The chronic exposure of air particulate matter from TRAP upon the vascular system leads to the enhancement of deposition of calcium in the vasculature leading to coronary artery calcification (CAC), triggered by inflammatory reactions and endothelial dysfunction. This calcification forms within the intimal and medial layers of vasculature and the underlying mechanism that connects the trigger from TRAP is not well explored. Several local and systemic factors participate in this active process including inflammatory response, hyperlipidemia, presence of self-programmed death bodies and high calcium-phosphate concentrations. These factors along with the loss of molecules that inhibit calcification and circulating nucleation complexes influence the development of calcification in the vasculature. The loss of defense to prevent osteogenic transition linked to micro organelle dysfunction that includes deteriorated mitochondria, elevated mitochondrial oxidative stress, and defective mitophagy. In this review, we examine the contributory role of mitochondria involved in the mechanism of TRAP linked CAC development. Further we examine whether TRAP is an inducer or trigger for the enhanced progression of CAC.