Complications of
vascular diseases, including
atherosclerosis, are the number one cause of death in Western societies. Dysfunction of endothelial cells is a critical underlying cause of the pathology of
atherosclerosis.
Lipid rafts, and especially caveolae, are enriched in endothelial cells, and down-regulation of the
caveolin-1 gene may provide protection against the development of
atherosclerosis. There is substantial evidence that exposure to environmental pollution is linked to cardiovascular mortality, and that
persistent organic pollutants can markedly contribute to endothelial cell dysfunction and an increase in vascular
inflammation. Nutrition can modulate the toxicity of
environmental pollutants, and evidence suggests that these affect health and disease outcome associated with chemical insults. Because caveolae can provide a regulatory platform for pro-inflammatory signalling associated with
vascular diseases such as
atherosclerosis, we suggest a link between atherogenic risk and functional changes of caveolae by environmental factors such as dietary
lipids and organic
pollutants. For example, we have evidence that endothelial caveolae play a role in uptake of
persistent organic pollutants, an event associated with subsequent production of inflammatory mediators. Functional properties of caveolae can be modulated by nutrition, such as dietary
lipids (e.g.
fatty acids) and plant-derived
polyphenols (e.g.
flavonoids), which change activation of caveolae-associated signalling
proteins. The following review will focus on caveolae providing a platform for pro-inflammatory signalling, and the role of caveolae in endothelial cell functional changes associated with environmental mediators such as nutrients and toxicants, which are known to modulate the pathology of
vascular diseases.