Calcification in atherosclerosis: bone biology and chronic inflammation at the arterial crossroads.

Dystrophic or ectopic mineral deposition occurs in many pathologic conditions, including atherosclerosis. Calcium mineral deposits that frequently accompany atherosclerosis are readily quantifiable radiographically, serve as a surrogate marker for the disease, and predict a higher risk of myocardial infarction and death. Accelerating research interest has been propelled by a clear need to understand how plaque structure, composition, and stability lead to devastating cardiovascular events.

The Stickler syndrome: genotype/phenotype correlation in 10 families with Stickler syndrome resulting from seven mutations in the type II collagen gene locus COL2A1.

Purpose: To evaluate a cohort of clinically diagnosed Stickler patients in which the causative mutation has been identified, determine the prevalence of clinical features in this group as a whole and as a function of age, and look for genotype/phenotype correlations.

Methods: Review of medical records, clinical evaluations, and mutational analyses of clinically diagnosed Stickler patients.

Results: Patients with seven defined mutations had similar phenotypes, though both inter- and intrafamilial variability were apparent and extensive.

Increased expression of membrane type 3-matrix metalloproteinase in human atherosclerotic plaque: role of activated macrophages and inflammatory cytokines.

Background: Matrix metalloproteinases (MMPs) are thought to play a prominent role in atherogenesis and destabilization of plaque. Pericellularly localized membrane-type (MT)-MMPs activate secreted MMPs. We investigated the hypothesis that MT3-MMP is expressed in human atherosclerotic plaques and is regulated by locally produced inflammatory cytokines and oxidized low-density lipoprotein (Ox-LDL).