The role of N6-methyladenosine methylation in environmental exposure-induced health damage.

Abstract

The health risks caused by environmental pollution have long been of substantial concern. With the development of epigenetics, a large number of studies have demonstrated that N6-methyladenosine (m6A) modification is involved in the regulation of various important life activities associated with various diseases. Recent studies have revealed that m6A plays a key role in health damage caused by environmental exposure by regulating post-transcriptional gene expression. Therefore, our study outlined the effects of environmental pollutant exposure on m6A methylation and its regulator levels. Moreover, we found that m6A methylation modifications were involved in the development of various health damages by regulating important life activities in vivo, such as reactive oxygen species imbalance, apoptosis, epithelial-mesenchymal transition (EMT), and inflammatory processes. More importantly, we delved into the regulatory mechanisms of m6A methylation dysregulation in environmental pollution-induced diseases. Finally, by examining the published literature, we found that methyltransferase-like protein 3 (METTL3) and fat mass- and obesity-associated protein (FTO) were potentially used as biomarkers of health damage induced by particulate matter exposure and heavy metal exposure, respectively. The current studies on regulators of METTL3 and FTO were more promising to bring new perspectives for the treatment of environmental health-related diseases.