Abstract
Lysophosphatidic acid and cardiovascular disease: seeing is believing
Highlights
In this issue of the Journal of Lipid Research, Bot and colleagues [1] provide further evidence that the bioactive lipid lysophosphatidic acid (LPA) accumulates in human and experimentally induced rodent atheromas and plays a role in the initiation and progression of atherothrombotic cardiovascular disease
LPA signaling can be terminated by enzymatic dephosphorylation catalyzed by members of the integral membrane cell surface lipid phosphate phosphatase (LPP) family [8] (Fig. 1)
Receptors, and pathways involved in LPA metabolism and signaling are involved in normal cardiovascular development and function and in experimental models of atherosclerosis has been provided by a series of studies from several groups combining genetic gain and loss of function approaches with the application of increasingly sophisticated pharmacological tools
Summary
In this issue of the Journal of Lipid Research, Bot and colleagues [1] provide further evidence that the bioactive lipid lysophosphatidic acid (LPA) accumulates in human and experimentally induced rodent atheromas and plays a role in the initiation and progression of atherothrombotic cardiovascular disease. LPA signaling can be terminated by enzymatic dephosphorylation catalyzed by members of the integral membrane cell surface lipid phosphate phosphatase (LPP) family [8] (Fig. 1). LPA disrupts the barrier function of cultured vascular endothelial cells and promotes the dedifferentiation, proliferation, and migration of vascular smooth muscle cells in vitro.
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