Chemokines in Atherosclerosis

Abstract

Chemokines play important roles in atherosclerotic vascular disease. Expressed by not only cells of the vessel wall but also emigrated leukocytes, chemokines were initially discovered to direct leukocytes to sites of inflammation. However, chemokines can also exert multiple functions beyond cell recruitment. Here, we discuss novel and recently emerging aspects of chemokines and their involvement in atherosclerosis. While reviewing newly identified roles of chemokines and their receptors in monocyte and neutrophil recruitment during atherogenesis and atheroregression, we also revisit homeostatic functions of chemokines, including their roles in cell homeostasis and foam cell formation. The functional diversity of chemokines in atherosclerosis warrants a clear-cut mechanistic dissection and stage-specific assessment to better appreciate the full scope of their actions in vascular inflammation and to identify pathways that harbor the potential for a therapeutic targeting of chemokines in atherosclerosis.

Chronic skin inflammation accelerates macrophage cholesterol crystal formation and atherosclerosis

“…Cytokines elevated in psoriasis patients include TNFα, IL12/23, IL1β, IFNγ, and IL17 (42) and are often targeted in a psoriasis treatment regimen. These cytokines have been demonstrated to be of crucial importance for macrophage plasticity in acute or chronic aspects and in regard to atherogenesis (11,19,43,44). However, since isolated macrophages in our study were differentiated under cytokine neutral conditions, a genetic preconditioning toward the proatherosclerotic phenotype may also modulate these characteristics.…”

Significant Association between Serum Monokine Induced by Gamma Interferon and Carotid Intima Media Thickness

“…Recent studies have suggested that pathologic T cell driven inflammatory responses play a key role in the progression of athero-. These T cell-related inflammatory responses involve interactions between cytokines, adhesion molecules, and chemokines 4,5) . Mach et al have demonstrated that T cell-activating C-X-C chemokines are highly expressed in human atheroma-associated cells throughout all stages of plaque development 6) .…”

T Cell CX3CR1 Mediates Excess Atherosclerotic Inflammation in Renal Impairment

“…13 Multiple chemokines have been implicated in this, including fractalkine receptor CX3CR1, which promotes lesion progression. 10,19 CX3CR1 is expressed on leukocytes, including monocytes, dendritic cells, T cells, and natural killer cells, 20 but also nonmyeloid cells such as aortic smooth muscle cells. 21 CX3CR1 deficiency (CX3CR1 2/2 , mostly studied in CX3CR1 gfp/gfp mice 22 ) decreases the development of atherosclerotic lesions in Apoe 2/2 mice.…”