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LPA is a component of oxidized low density lipoproteins (oxLDL) which has been shown to accumulate in human atherosclerotic plaques. Tissue factor (TF) is the principal initiator of blood coagulation. Tissue factor upregulation in atherosclerotic plaque can lead to undesirable vascular thrombosis. The generation of reactive oxygen species (ROS), which act as signaling molecules in the vascular system, is enhanced in response to injury and has been associated with a procoagulant state and the progression of atherosclerotic disease. Oxidative stress might contribute to the increased expression…mehr

Produktbeschreibung
LPA is a component of oxidized low density lipoproteins (oxLDL) which has been shown to accumulate in human atherosclerotic plaques. Tissue factor (TF) is the principal initiator of blood coagulation. Tissue factor upregulation in atherosclerotic plaque can lead to undesirable vascular thrombosis. The generation of reactive oxygen species (ROS), which act as signaling molecules in the vascular system, is enhanced in response to injury and has been associated with a procoagulant state and the progression of atherosclerotic disease. Oxidative stress might contribute to the increased expression of pro atherosclerotic genes at sites of vascular injury, including TF. Little is known about the regulation of TF by LPA in smooth muscle cells (SMC) which is a major player in the process of atherosclerosis. Data generated by this study demonstrate that LPA markedly induces TF expression in rat aorta smooth muscle cells (RASMCs) and human aorta smooth muscle cells (HASMCs). The signaling pathways involved are multiple.
Autorenporträt
Essam Laag was born in Tanta-Egypt in 1962. He graduated from Tanta University Faculty of Medicine, Egypt. He received his Ph.D in comparative and Experimental Medicine at the university of Tennessee in 2000. He is presently a lecturer in the department of Histology at the College of Medicine, University of Tanta, Egypt.