Diffuse calcification in human coronary arteries. Association of osteopontin with atherosclerosis.

Fitzpatrick, Lorraine A.; Severson, Arlen R.; Edwards, William D.; Ingram, Ronald T.

doi:10.1172/jci117501

Cited by 343 publications

(194 citation statements)

References 31 publications

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“…These osteoblastic reactions may then lead to mineralization of the extracellular matrix. [7][8][9][10][11] Witko-Sarsat et al were the first to report that AOPPs were significantly increased in hemodialysis patients and proposed that AOPPs might be formed during oxidative stress by reaction of plasma proteins with chlorinated oxidants. AOPPs have been recognized as markers of oxidant-mediated protein damage.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6] Accumulating evidence suggests that vascular calcification resembles developmental bone mineralization, with the production of "bone" proteins by vascular smooth muscle cells (VSMCs), such as osteopontin (OPN) and type-I collagen. [7][8][9][10][11] Furthermore, a recent study [12] demonstrates that the addition of uremic serum to cultured VSMCs accelerated mineralization and up-regulated the expression of osteopontin and core binding factor-a1 (CBF-a1), a transcription factor that is important for osteoblast differentiation and bone matrix protein expression. [13] This implies that the uremia may lead to dedifferentiation of VSMCs, with subsequent mineralization.…”

Section: Introductionmentioning

confidence: 99%

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Advanced Oxidation Protein Products Induce Vascular Calcification by Promoting Osteoblastic Trans-Differentiation of Smooth Muscle Cells via Oxidative Stress and ERK Pathway

et al. 2009

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Vascular calcification is an actively regulated process similar to bone formation. Advanced oxidation protein products (AOPPs) have been demonstrated to be novel markers of oxidantmediated protein damage. The present study investigated the role of AOPPs in inducing osteoblastic trans-differentiation and calcification of smooth muscle cells in vitro. We found that AOPPs directly increased the calcium deposition and expression of core binding factor-a1 (CBF-a1) and osteopontin (OPN) and significantly decreased SM-a-actin expression in human aortic smooth muscle cells (HASMCs). AOPPs increased intracellular oxidative stress, which was inhibited by vitamin E. Vitamin E also inhibited AOPP-induced calcium content and osteoblast differentiation of HASMCs. Furthermore, the inhibitor of ERK significantly suppressed the effects of AOPPs on calcification and osteoblast marker expression. These findings suggest that AOPPs induce vascular calcification by promoting osteoblast differentiation of smooth muscle cells via oxidative stress and ERK pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Advanced Oxidation Protein Products Induce Vascular Calcification by Promoting Osteoblastic Trans-Differentiation of Smooth Muscle Cells via Oxidative Stress and ERK Pathway

et al. 2009

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“…However, this finding does not rule out a role for OPN in preventing mineral precipitation in atherosclerotic arteries. OPN is not found in normal arteries but is indeed expressed in plaque and colocalizes with calcified plaque regions (23). It is therefore possible that OPN might play a protective role where necessary and be expressed in plaque only in response to local conditions that might tend to favor mineralization.…”

Section: Passive Model Of Arterial Calcificationmentioning

confidence: 99%

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

Doherty

Asotra

Fitzpatrick

et al. 2003

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

405

320

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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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“…9 In contrast to the commonly held theory that coronary calcium is a degenerative process, its participation in atherosclerotic plaque development is active and regulated in a fashion similar to bone mineralization. 9,[20][21][22][23] Although its role in coronary disease remains unclear, intramural calcium can be variably Fig. 1.…”

Section: Calcium Atherosclerotic Plaque and Extent Of Diseasementioning

confidence: 99%

Electron Beam Computed Tomographic Coronary Calcium Scanning: A Review and Guidelines for Use in Asymptomatic Persons

Rumberger

Brundage²,

Rader

et al. 1999

Mayo Clinic Proceedings

742

449

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Diffuse calcification in human coronary arteries. Association of osteopontin with atherosclerosis.

Abstract: IntroductionCoronary atherosclerosis is frequently associated with calcification of arterial plaque.

Cited by 343 publications

References 31 publications

Advanced Oxidation Protein Products Induce Vascular Calcification by Promoting Osteoblastic Trans-Differentiation of Smooth Muscle Cells via Oxidative Stress and ERK Pathway

Advanced Oxidation Protein Products Induce Vascular Calcification by Promoting Osteoblastic Trans-Differentiation of Smooth Muscle Cells via Oxidative Stress and ERK Pathway

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

Electron Beam Computed Tomographic Coronary Calcium Scanning: A Review and Guidelines for Use in Asymptomatic Persons

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