Clinical, cellular, and molecular aspects of arterial calcification
Received 19 January 2007; accepted 17 February 2007.
Arterial calcification is a complex and independently regulated process with risk factors similar to those for atherosclerotic occlusive disease. It may develop either within the atherosclerotic intima or in the media. When calcification is found in coronary or lower extremity arteries, it is an independent predictor of cardiovascular events and lower extremity amputation. Recent evidence suggests a role for several endogenous stimulators and inhibitors in the pathogenesis of arterial calcification. Inflammatory mediators and matrix-degrading enzymes are also thought to control the progression of calcification in humans. Current research involves efforts to define the complex interactions between cellular and molecular mediators of arterial calcification.
Department of Surgery, Division of Vascular Surgery, Vanderbilt University Medical Center, Nashville, Tenn.
Reprint requests: Raul J. Guzman, MD, Department of Surgery, Division of Vascular Surgery, Vanderbilt University Medical Center, D-5237 MCN Bldg, 1161 21st Ave So, Nashville, TN 37235.
This research was supported by a Mentored Clinical Scientist Development Award from the NIH HL069926, a grant from the NIDDK DK067368, and grants from the Lifeline Foundation, and the William J. von Liebig Foundation.