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Does the coronary risk factor low density lipoprotein alter growth and signaling in vascular smooth muscle cells?

Medical Clinic II, University of Cologne, 50931 Cologne, Germany; and
^* Center of Physiology and Pathophysiology, University of Cologne, 50931 Cologne, Germany

¹Correspondence: Center of Physiology and Pathophysiology, University of Cologne, Robert-Koch Str. 39, 50931 Cologne, Germany. E-mail: A.Sachinidis{at}uni-koeln.de

There is increasing evidence that hypertension promotes low density lipoprotein (LDL) transportation into the subendothelial space of the vascular wall. Vascular smooth muscle cell (VSMC) proliferation plays an important role in the development and progression of cardiovascular diseases. Recently, several studies have demonstrated that LDL acts as a classic growth factor promoting VSMC growth via mitogenic signals normally elicited by classic growth factors. The present work summarizes current nontraditional concepts regarding possible cellular mechanisms through which hypertension and LDL may promote the development of atherosclerosis. Especially addressed are the possible effects of an elevated blood pressure in combination with LDL on VSMC growth. The new research concept concerning LDL as a growth factor and carrier for biological active phospholipids such as sphingosine-1-phosphate and sphingosylphosphorylcholine may contribute to an understanding of the pathogenesis of atherosclerosis by elevated high blood pressure—Gouni-Berthold, I., Sachinidis, A. Does the coronary risk factor low density lipoprotein alter growth and signaling in vascular smooth muscle cells?

Key Words: LDL • atherosclerosis • hypertension • signal transduction • MAP kinases • sphingosine-1-phosphate

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