Adverse effects of ambient fine particulate matter (PM_2.5) on vascular smooth muscle cells

Abstract

Cardiovascular diseases are the leading cause of death worldwide. Meanwhile, environment air pollution has become a serious health risk factor, contributing to the mortality of respiratory and cardiovascular diseases. A substantial body of evidence has shown that many types of vascular diseases are related to air pollution. The physiology and pathophysiology of the three layers of vascular vessels, especially the inner and medial layer, contribute to the process of vascular diseases. Vascular smooth muscle cells (VSMCs) are the predominant cells in the medial layer, and several studies have indicated that air pollution has an adverse effect on VSMCs. There are numerous sources of air pollution across the world, and the components of air pollutants are a complex mixture of gaseous pollutants and particulate matter. Among these air pollutants, particulate matter (PM)2.5 presents the highest risk factor leading to global mortality from cardiovascular disease and disability. In this review, we primarily focus on the impacts of PM2.5 exposure on VSMCs. We further discuss the correlation between exposure to PM2.5 and other vascular diseases and present potential protective and treatment strategies to decrease vascular mortality related to air pollution.

Wildland fire, air pollution and cardiovascular health: is it time to focus on the microvasculature as a risk assessment tool?

“…Limited literature exists regarding the impact of PM from wildland fire smoke on vascular smooth muscle cells (VSMCs). As reviewed by Ming and colleagues, the impact of PM 2.5 on VSMCs has been mainly investigated for particles originating from cigarette smoke, diesel exhaust, or urban airborne pollution but not wildland fires and other biomass burning ( Ming et al, 2022 ). In addition, most of these studies have used smooth muscle cells from macrovascular origin (i.e., isolated from aorta) with an interest in studying whether PM could promote atherosclerosis through the activation of smooth muscle hypertrophy ( Chang et al, 2017 ; Wan et al, 2018 ; Ho et al, 2019 ; Gu et al, 2021 ; Ho et al, 2021 ; Tian et al, 2021 ; Ju et al, 2022 ; Ming et al, 2022 ; Bao et al, 2023 ).…”

“…As reviewed by Ming and colleagues, the impact of PM 2.5 on VSMCs has been mainly investigated for particles originating from cigarette smoke, diesel exhaust, or urban airborne pollution but not wildland fires and other biomass burning (Ming et al, 2022). In addition, most of these studies have used smooth muscle cells from macrovascular origin (i.e., isolated from aorta) with an interest in studying whether PM could promote atherosclerosis through the activation of smooth muscle hypertrophy (Chang et al, 2017;Wan et al, 2018;Ho et al, 2019;Gu et al, 2021;Ho et al, 2021;Tian et al, 2021;Ju et al, 2022;Ming et al, 2022;Bao et al, 2023). Similarly to cigarette smokerelated PM, particles from urban pollution increase mitogenic and hypertrophic signals (e.g., PDGFR-β, JAK2/STAT3) in macrovascular VSMCs, promoting the thickening of the media, an contributing to atherosclerosis and calcification in the aorta (Bao et al, 2023;Schroeter et al, 2008;R;Li et al, 2013).…”