Acting through cell surface receptors, “extracellular” lysophosphatidic acid (LPA) influences cell growth, differentiation, apoptosis and development in a wide spectrum of settings [–5]. Within the vasculature, smooth muscle cells [6, 7], endothelial cells  and platelets [9, 10] display notable responses to LPA [11, 12], which likely regulate blood vessel development and contribute to vascular pathology. The bioactive effects of LPA are mediated by a family of G-protein coupled receptors with at least six members (termed LPA1-6 that are encoded by the LPAR genes in humans and Lpar in mice) [–3]. LPA may also serve as a ligand for the receptor for advanced glycation end products (RAGE) . This review summarizes evidence to support a role for LPA signaling in vascular biology based on studies of LPA receptors and enzymes that produce or metabolize the lipid (Figure 1).
Keywords: Atherosclerosis; Autotaxin; Endothelial cells; Lipid phosphate phosphatase; Lysophosphatidic acid; Smooth muscle cells.