The effects of cytokines on the atherosclerotic process

Atherosclerotic lesions result from a series of highly specific cellular and molecular responses to various endogenous risk factors and potential exogenous antigens. The cellular mechanisms involved in atherogenesis, with the exception of calcification and thrombotic events, are principally no different to those found in chronic inflammatory fibroproliferative diseases such as liver cirrhosis, rheumatoid arthritis, glomerulosclerosis, pulmonary fibrosis or chronic pancreatitis. These responses are mediated by interactions among endothelial cells, monocyte-derived macrophages, smooth muscle cells and specific subtypes of T lymphocytes. Monocyte and lymphocyte activation leads to the release of a wide spectrum of cytokines and chemokines that have key roles in all of the phases of endothelial damage, as well as in the formation and rupture of the atherosclerotic plaques. This review attempts to analyze the role of chemokines and cytokines in the multiple steps of atherosclerotic process.