Abstract
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.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Bone Resorption
-
Calcinosis / epidemiology
-
Calcinosis / metabolism*
-
Calcinosis / pathology
-
Calcinosis / physiopathology
-
Calcium / metabolism*
-
Coronary Artery Disease / epidemiology
-
Coronary Artery Disease / metabolism*
-
Coronary Artery Disease / pathology
-
Coronary Artery Disease / physiopathology
-
Disease Models, Animal
-
Extracellular Matrix Proteins / metabolism
-
Fibroblasts / metabolism
-
Fibroblasts / pathology
-
Humans
-
Inflammation Mediators / metabolism
-
Matrix Metalloproteinases / metabolism
-
Mesenchymal Stem Cells / metabolism
-
Mesenchymal Stem Cells / pathology
-
Mice
-
Myocytes, Smooth Muscle / metabolism
-
Myocytes, Smooth Muscle / pathology
-
Pericytes / metabolism
-
Pericytes / pathology
-
Peripheral Vascular Diseases / epidemiology
-
Peripheral Vascular Diseases / metabolism*
-
Peripheral Vascular Diseases / pathology
-
Peripheral Vascular Diseases / physiopathology
-
Phenotype
-
Phosphorus / metabolism
-
Risk Factors
-
Signal Transduction*
Substances
-
Extracellular Matrix Proteins
-
Inflammation Mediators
-
Phosphorus
-
Matrix Metalloproteinases
-
Calcium