Macrophage glucocorticoid receptors join the intercellular dialogue in atherosclerotic lesion calcification.

Arterial calcification is one of the potential phenotypes of vascular remodeling and repair in atherosclerosis, diabetes, hyperphosphatemic renal failure, and aging.1–3 Calcification decreases arterial wall compliance.4 Furthermore, deposited crystalline apatite can activate macrophages, resulting in a proinflammatory phenotype. Consequently, arterial calcification localized to the intima is a potential biomarker of atherosclerosis and is linked to disease progression and cardiovascular mortality, whereas arterial calcification localized primarily to the tunica media promotes mortality in diabetes and renal failure.4 In addition, calcific stenosis of the aortic valve is a prevalent and highly significant public health problem, and shares such pathophysiological features as ectopic chondroosseous differentiation in common with arterial calcification.5