Inhibition of bone morphogenetic protein signaling reduces vascular calcification and atherosclerosis.

Cyclic strain induces dual-mode endothelial-mesenchymal transformation of the cardiac valve.

Look more closely at the valve: imaging calcific aortic valve disease.

Liberation of desmosine and isodesmosine as amino acids from insoluble elastin by elastolytic proteases.

Selective inhibition of matrix metalloproteinase-13 increases collagen content of established mouse atherosclerosis.

Statin-induced Krüppel-like factor 2 expression in human and mouse T cells reduces inflammatory and pathogenic responses.

Intimal smooth muscle cells: the context-dependent origin.

High-resolution magnetic resonance imaging enhanced with superparamagnetic nanoparticles measures macrophage burden in atherosclerosis.

Genetically engineered resistance for MMP collagenases promotes abdominal aortic aneurysm formation in mice infused with angiotensin II.

Free cholesterol accumulation in macrophage membranes activates Toll-like receptors and p38 mitogen-activated protein kinase and induces cathepsin K.

Arterial and aortic valve calcification abolished by elastolytic cathepsin S deficiency in chronic renal disease.

Matrix-metalloproteinase-14 deficiency in bone-marrow-derived cells promotes collagen accumulation in mouse atherosclerotic plaques.

Increased plasma oxidized phospholipid:apolipoprotein B-100 ratio with concomitant depletion of oxidized phospholipids from atherosclerotic lesions after dietary lipid-lowering: a potential biomarker of early atherosclerosis regression.

Delta-like 4 induces notch signaling in macrophages: implications for inflammation.

Osteogenesis associates with inflammation in early-stage atherosclerosis evaluated by molecular imaging in vivo.

The balance of power: the law of Yin and Yang in smooth muscle cell fate. Is YY1 a vascular protector?

Human semilunar cardiac valve remodeling by activated cells from fetus to adult: implications for postnatal adaptation, pathology, and tissue engineering.

Inflammation in atherosclerosis: visualizing matrix metalloproteinase action in macrophages in vivo.

Matrix metalloproteinase-13/collagenase-3 deletion promotes collagen accumulation and organization in mouse atherosclerotic plaques.

Hypochlorous acid, a macrophage product, induces endothelial apoptosis and tissue factor expression: involvement of myeloperoxidase-mediated oxidant in plaque erosion and thrombogenesis.

Genetically determined resistance to collagenase action augments interstitial collagen accumulation in atherosclerotic plaques.

The vulnerable atherosclerotic plaque: pathogenesis and therapeutic approach.

Direct anti-inflammatory mechanisms contribute to attenuation of experimental allograft arteriosclerosis by statins.

Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction.

Lipid lowering reduces oxidative stress and endothelial cell activation in rabbit atheroma.

Stabilization of atherosclerotic plaques: new mechanisms and clinical targets.

Vitamin C, collagen, and cracks in the plaque.

Biomechanical strain induces class a scavenger receptor expression in human monocyte/macrophages and THP-1 cells: a potential mechanism of increased atherosclerosis in hypertension.

Host bone-marrow cells are a source of donor intimal smooth- muscle-like cells in murine aortic transplant arteriopathy.

Activated interstitial myofibroblasts express catabolic enzymes and mediate matrix remodeling in myxomatous heart valves.

An HMG-CoA reductase inhibitor, cerivastatin, suppresses growth of macrophages expressing matrix metalloproteinases and tissue factor in vivo and in vitro.

Statins alter smooth muscle cell accumulation and collagen content in established atheroma of watanabe heritable hyperlipidemic rabbits.

Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction.

Echocardiography-derived left ventricular end-systolic regional wall stress and matrix remodeling after experimental myocardial infarction.

MRI of rabbit atherosclerosis in response to dietary cholesterol lowering.

Dietary lipid lowering reduces tissue factor expression in rabbit atheroma.

Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma: a potential mechanism of lesion stabilization.

Lipid lowering promotes accumulation of mature smooth muscle cells expressing smooth muscle myosin heavy chain isoforms in rabbit atheroma.

Redifferentiation of smooth muscle cells after coronary angioplasty determined via myosin heavy chain expression.

Isolation of the embryonic form of smooth muscle myosin heavy chain (SMemb/NMHC-B) gene and characterization of its 5'-flanking region.

Nonmuscle and smooth muscle myosin heavy chain expression in rejected cardiac allografts. A study in rat and monkey models.

Ductus arteriosus. Advanced differentiation of smooth muscle cells demonstrated by myosin heavy chain isoform expression in rabbits.

Human smooth muscle myosin heavy chain isoforms as molecular markers for vascular development and atherosclerosis.

Chronic hypoxia activates the Akt and beta-catenin pathways in human macrophages.

Crosstalk between macrophages and smooth muscle cells in atherosclerotic vascular diseases.

The osteoclast-associated receptor (OSCAR) is a novel receptor regulated by oxidized low-density lipoprotein in human endothelial cells.

Prostaglandin E receptor type 4-associated protein interacts directly with NF-kappaB1 and attenuates macrophage activation.

Transglutaminase activity in acute infarcts predicts healing outcome and left ventricular remodelling: implications for FXIII therapy and antithrombin use in myocardial infarction.

Inhibited aortic aneurysm formation in BLT1-deficient mice.

Characterization of smooth muscle-like cells in circulating human peripheral blood.