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Deletion of the lysophospholipid-sensitive receptor, G2A, in low-density lipoprotein receptor knockout (LDLR(-/-)) mice elevates plasma high-density lipoprotein (HDL) cholesterol and suppresses atherosclerosis. However, chemotactic action of G2A in monocytes/macrophages, in addition to its modulatory effect on HDL, may contribute to the proatherogenic action of G2A.

ApoE-Dependent Modulation of HDL and Atherosclerosis by G2A in LDL Receptor–Deficient Mice Independent of Bone Marrow–Derived Cells