The macrophage senescence hypothesis: the role of poor heat shock response in pulmonary inflammation and endothelial dysfunction following chronic exposure to air pollution.

, we suppose that the pollutant impairs HSR and, consequently, induces cellular senescence. Accordingly, senescent macrophages change its secretory phenotype to a more inflammatory one, known as SASP. Finally, macrophages' SASP would propagate the systemic inflammation, leading to endothelial dysfunction and atherosclerosis.