Atherosclerosis is an inflammatory disease and hyperlipidaemia is one of the main risk factors for aging,
hypertension and diabetes. Variance in plasma
LDL cholesterol concentration may be associated with differences in
cardiovascular disease risk and high levels of
lipids are associated with increased risk of developing
atherosclerosis. Macrophages, which generate pro-inflammatory
cytokines, mainly
interleukin-1 (IL-1) and
tumor necrosis factor-α (
TNF-alpha), are deeply involved in
atherosclerosis, as well as mast cells which generate several
cytokines, including
IL-6 and IFN-gamma, and
chemokines such as eotaxin, MCP-1 and
RANTES involved in monocyte recruitment and differentiation in the arterial wall. In addition, mast cells participate in
lipid retention and vascular cell remodeling, and are mediators of innate and adaptive immunity during
atherosclerosis. Mast cells which accumulate in the human arterial intima and adventitia during
atherosclerotic plaque progression, release vasoactive and angiogenic compounds, and pro-inflammatory mediators, such as
arachidonic acid metabolites,
histamine,
cytokines/
chemokines,
platelet activating factor (PAF) and
proteolytic enzymes. Mast cells can be activated by pro-inflammatory stimuli, including
cytokines,
hypercholesterolemia, and
hyperglycemia, and trigger the endothelial expression of adhesion molecules such as P-selection,
vascular cell adhesion molecule-1 (VCAM-1) and
chemokines which mediate the recruitment and adhesion of leukocytes. The participation of mast cells in
atherosclerosis is still an enigma and it may be of therapeutic interest to clarify this process.