Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE mice exposed to diesel exhaust particles.

Air pollution is an environmental risk factor linked to multiple human diseases including cardiovascular diseases (CVDs). While particulate matter (PM) emitted by diesel exhaust damages multiple organ systems, heart disease is one of the most severe pathologies affected by PM. However, the in vivo effects of diesel exhaust particles (DEP) on the heart and the molecular mechanisms of DEP-induced heart dysfunction have not been investigated.

Diesel exhaust particles induce human umbilical vein endothelial cells apoptosis by accumulation of autophagosomes and caspase-8 activation.

Diesel exhaust particles (DEP) are risk factors for endothelial cells (ECs) dysfunction. However, the mechanism by which DEP induce ECs apoptosis remains unclear. Here, we investigated how DEP induce death of human umbilical vein ECs (HUVECs), with a focus on the autophagy-mediated apoptotic pathway.

Transcriptional analysis of gasoline engine exhaust particulate matter 2.5-exposed human umbilical vein endothelial cells reveals the different gene expression patterns related to the cardiovascular diseases.

Particulate matter (PM) causes several diseases, including cardiovascular diseases (CVDs). Previous studies compared the gene expression patterns in airway epithelial cells and keratinocytes exposed to PM. However, analysis of differentially expressed gene (DEGs) in endothelial cells exposed to PM2.