The influence of PM2.5 exposure on non-alcoholic fatty liver disease

Emerging studies have pointed to a significant relationship between exposure to ambient fine particulate matter (aerodynamic diameter < 2.5 mu m, PM2.5) and the incidence of non-alcoholic fatty liver disease (NAFLD). By referring to previous studies on the pathogenesis of NAFLD and PM2.5 exposure-induced metabolic damage, we summarized the possible mediating pathways through which PM2.5 exposure can cause the phenotype and progression of NAFLD. Crucially, PM2.5 exposure is considered to have an impact on the classic hypothesis multiple hits of NAFLD. In addition, we also concluded that exposure to PM2.5 can promote the development of NAFLD by destroying the intestinal epithelium and microbiotic homeostasis, triggering endoplasmic reticulum stress, inducing abnormal expression of specific microRNA or inflammatory factors.

Automated summary

Exposure to PM2.5 is significantly related to the incidence of NAFLD, impacting the classic multiple hits hypothesis and promoting disease development through pathways such as disrupting intestinal epithelium, triggering endoplasmic reticulum stress, and inducing abnormal expression of specific microRNA or inflammatory factors.