Atherosclerosis

1980

DOI: 10.1016/0021-9150(80)90005-2

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Chemical and physicochemical studies on the mineral deposits of the human atherosclerotic aorta

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William O. McSharry

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Cornelis H. Pameijer

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et al.

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Discussion2

Atherosclerotic Calcification1

Active Model Versus Passive Model Of Arterial Calcification1

Introduction1

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1998

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Cited by 186 publications

(99 citation statements)

References 7 publications

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“…The association of vascular calcification with osteoporosis in patient populations is a recognized phenomenon (Banks et al 1994; Parhami and Demer 1997; Postnatal osteoporosis in OPG-deficient mice . The mineral within calcified plaques in the vasculature has been determined to be hydroxyapatite, the same mineral found in bone (Schmid et al 1980). Additionally, calcified arteries have been shown to express several bone matrix proteins, including collagen type I, matrix GLA protein, osteocalcin, osteonectin, and bone morphogenetic protein type 2, raising the possibility that dysregulation of vessel wall protein and/or growth factor synthesis by smooth muscle or other cells leads to vessel wall calcification.…”

Section: Discussionmentioning

confidence: 99%

osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification

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et al. 1998

Genes & Development

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Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG −/− mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.

“…The association of vascular calcification with osteoporosis in patient populations is a recognized phenomenon (Banks et al 1994; Parhami and Demer 1997; Postnatal osteoporosis in OPG-deficient mice . The mineral within calcified plaques in the vasculature has been determined to be hydroxyapatite, the same mineral found in bone (Schmid et al 1980). Additionally, calcified arteries have been shown to express several bone matrix proteins, including collagen type I, matrix GLA protein, osteocalcin, osteonectin, and bone morphogenetic protein type 2, raising the possibility that dysregulation of vessel wall protein and/or growth factor synthesis by smooth muscle or other cells leads to vessel wall calcification.…”

Section: Discussionmentioning

confidence: 99%

osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification

¹

,

et al. 1998

Genes & Development

View full text Add to dashboard Cite

Osteoprotegerin (OPG) is a secreted protein that inhibits osteoclast formation. In this study the physiological role of OPG is investigated by generating OPG-deficient mice. Adolescent and adult OPG −/− mice exhibit a decrease in total bone density characterized by severe trabecular and cortical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fractures. These findings demonstrate that OPG is a critical regulator of postnatal bone mass. Unexpectedly, OPG-deficient mice also exhibit medial calcification of the aorta and renal arteries, suggesting that regulation of OPG, its signaling pathway, or its ligand(s) may play a role in the long observed association between osteoporosis and vascular calcification.

“…118 Histologically, intimal calcification is observed as hydroxyapatite crystals originating from secreted matrix vesicles in the vicinity of the lipid rich necrotic core and in close proximity to cellular debris and inflammatory cell infiltrate. 117,119,120 Since hydroxyapatite crystals are propagated along extracellular matrix fibers, the composition of the extracellular matrix has a profound effect in regulating this process, and collagens, which are abundant in atherosclerotic lesions, are likely to contribute to intimal calcification.…”

Section: Atherosclerotic Calcificationmentioning

confidence: 99%

Collagens in the progression and complications of atherosclerosis

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et al. 2009

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Collagens constitute a major portion of the extracellular matrix in the atherosclerotic plaque, where they contribute to the strength and integrity of the fibrous cap, and also modulate cellular responses via specific receptors and signaling pathways. This review focuses on the diverse roles that collagens play in atherosclerosis; regulating the infiltration and differentiation of smooth muscle cells and macrophages; controlling matrix remodeling through feedback signaling to proteinases; and influencing the development of atherosclerotic complications such as plaque rupture, aneurysm formation and calcification. Expanding our understanding of the pathways involved in cell-matrix interactions will provide new therapeutic targets and strategies for the diagnosis and treatment of atherosclerosis.

“…Atherosclerosis involves both chronic inflammation and necrosis. Atherosclerotic arteries, however, may also contain bonelike tissues, including hematopoietic tissue (2) and hydroxyapatite (10). These features distinguish atherosclerotic arterial calcification from the dystrophic calcium deposition frequently observed in conditions involving chronic inflammation and necrosis and also from other types of vascular calcification, such as calcification of the medial layer of the artery.…”

Section: Active Model Versus Passive Model Of Arterial Calcificationmentioning

confidence: 99%

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

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²

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et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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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. In atherosclerotic plaque, accumulating evidence is consistent with the notion that calcification involves the participation of arterial osteoblasts and osteoclasts. Here we summarize current models of intimal arterial plaque calcification and highlight intriguing questions that require further investigation. Because atherosclerosis is a chronic vascular inflammation, we propose that arterial plaque calcification is best conceptualized as a convergence of bone biology with vascular inflammatory pathobiology.P laque structure and composition importantly impact clinical expression of atherosclerosis. Molecular medicine in the 21st century has turned toward a comprehensive understanding of the dynamic processes that influence the composition and stability of atheroma and of how structural plaque components impact clinical outcomes. Recently, increasing interest has focused on understanding how atherosclerotic pathology is related to a common plaque constituent: calcium mineral deposits. Pathologists have long known that calcified atherosclerotic arteries can contain tissue that is histomorphologically indistinguishable from bone (1, 2). Important studies in the last decade have now spawned a model wherein calcification in atherosclerotic plaque is viewed as an active, complex, and therefore presumably regulated process that exhibits intriguing similarities to new bone formation, or remodeling. Ectopic and dystrophic mineral deposition and extracellular matrix calcification can occur in numerous pathologic conditions by passive precipitation. Here we focus on one specific type of mineral deposition with high relevance to cardiac pathology: intimal arterial calcification in the context of atherosclerotic plaque. The emerging view is that plaque calcification represents a meeting of bone biology with chronic plaque inflammation. Remarkable cellular ontogenetic versatility in atherosclerosis appears to effect profound structural alterations, with significant ramifications for plaque stability and clinical outcomes. Clinical SignificanceAtherosclerotic lesions frequently become calcified. The process can begin early and accelerates as the disease progresses and more complex lesions develop. Calcium deposits in coronary arteries indicate the presence of plaque, but the converse statement that an absence of coronary calcium indicates an absence of atheromatous plaque is not true (1). Because calcification is a surrogate measure of coronary atherosclerosis, clinical interest has focused on the usefulness of noninvasive detection of calci...

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