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Aside from its impact on HDL and other plasma lipids, nicotinic acid has exhibited anti-atherosclerotic activities in cultured monocytes, macrophages, or vascular endothelial cells, by modulating inflammation and oxidative stress and regulating cell adhesion, migration, and differentiation (reviewed in 18)

The noxious chemicals present in tobacco smoke are also known to cause inflammation and associated lung injury (22, 23), but its role in CTD-ILD is not clearly established