Free fatty acid overload attenuates Ca2+ signaling and NO production in endothelial cells.

Hyperlipidemia represents a major risk factor for development of vascular dysfunction and atherosclerosis. Although the unfortunate role of low-density lipoprotein has been clearly demonstrated, the mechanistic pathways through which triglyceride-derived free fatty acids (FFAs) contribute to vascular disorders are not completely understood. Thus, the present study was designed to elucidate the effects of FFAs on cultured endothelial cells.

Tissue-specific expression of human lipoprotein lipase in the vascular system affects vascular reactivity in transgenic mice.

1. The role of smooth muscle-derived lipoprotein lipase (LPL) that translocates to the endothelium surface on vascular dysfunction during atherogenesis is unclear. Thus, the role of vascular LPL on blood vessel reactivity was assessed in transgenic mice that specifically express human LPL in the circulatory system.