PM2.5 exposure induces vascular dysfunction via NO generated by iNOS in lung of ApoE-/- mouse

Citations Over TimeTop 19% of 2019 papers

Abstract

PM2.5 exposure exacerbates cardiovascular diseases via oxidative stress and inflammation, the detailed mechanism of which is unclear. In this study, the effects of oxidative stress and inflammation, as well as vascular structure and function were studied by multiple PM2.5 exposure model of ApoE-/- mice. The results indicated that NO produced by iNOS not cNOS might play important roles in inducing vascular dysfunction after PM2.5 exposure. The occurrence order and causality among NO, other oxidative stress indicators and inflammation is explored by single PM2.5 exposure. The results showed that NO generated by iNOS occurred earlier than that of other oxidative stress indicators, which was followed by the increased inflammation. Inhibition of NOS could effectively block the raise of NO, oxidative stress and inflammation after PM2.5 exposure. All in all, we firstly confirmed that NO was the initiation factor of PM2.5 exposure-induced oxidative stress, which led to inflammation and the following vascular dysfunction.

Related Papers

• → Oxidative stress and mitochondrial dysfunction in glaucoma(2012)387 cited
• → Oxidative Stress in Relation to Aging and Exercise(2022)25 cited
• → Myocardial bridging and endothelial dysfunction – Computational fluid dynamics study(2019)13 cited
• Endothelial Dysfunction and Hypertension(2009)
• Susquehanna Chorale Spring Concert "Roots and Wings"(2017)