PM2.5 pollution and endoplasmic reticulum stress response

Abstract

Air pollution is a sustained problem of public health for the general population in urban areas, especially for those living in areas of intensive traffic or industrial activity. Accumulating evidence has confirmed a significant association between exposure to fine ambient particulate matter with aerodynamic diameters <2.5 μm (PM2.5) and the increase of morbidity and mortality associated with cardiovascular and metabolic diseases. It has been identified that inflammation and intracellular stress responses play important roles in PM2.5-caused pathogenesis. Unfolded protein response (UPR) is an intracellular stress signaling from the endoplasmic reticulum (ER) to help cell recovery from the stress caused by the accumulation of unfolded or misfolded proteins. Exposure to high levels of environmentally relevant PM2.5 may directly or indirectly interrupt the protein folding process in the ER, causing ER stress. A number of studies suggested that ER stress response, or UPR, interacts with mitochondrial stress and inflammatory responses, under PM2.5 exposure, to modulate functions and survival of specialized cell types that are involved in the development of cardiovascular, metabolic, and neurodegenerative diseases. In this review, we summarize the recent advance in understanding the mechanistic links between PM2.5 and ER stress response.