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Chemokines are a family of low-molecular-weight proteins essential to the directed migration of cells under homeostatic and pathological conditions. Fractalkine (CX3CL1) is an unusual chemokine that can act as either a soluble or membrane-bound mediator and signals through the G protein-coupled chemokine receptor CX3CR1, expressed on monocytes, natural killer cells, T cells, and smooth muscle cells. Accumulating evidence suggests that fractalkine, in addition to its role in chemotaxis and adhesion of leukocytes, supports the survival of multiple cell types during homeostasis and inflammation. This review presents the evidence obtained from several disease models implying an antiapoptotic function for fractalkine and shows how this is relevant to the pathology of atherosclerosis and other vascular diseases. We discuss whether the key role of fractalkine, unlike other chemokines, is the promotion of cell survival and whether this has implications for vascular disease.

Original publication

DOI

10.1161/ATVBAHA.111.237412

Type

Journal article

Journal

Arterioscler Thromb Vasc Biol

Publication Date

03/2012

Volume

32

Pages

589 - 594

Keywords

Animals, Apoptosis, Asthma, Atherosclerosis, Cell Survival, Chemokine CX3CL1, Diabetes Mellitus, Hepatitis, Humans, Inflammation, Myeloid Cells, Receptors, Chemokine, Signal Transduction, T-Lymphocytes