Contribution of localized calcium deposits to dissection after angioplasty. An observational study using intravascular ultrasound.

Fitzgerald, Peter J.; Ports, Thomas A.; Yock, Paul G.

doi:10.1161/01.cir.86.1.64

Cited by 478 publications

(225 citation statements)

References 24 publications

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“…However, the introduction of new techniques to measure vascular calcification noninvasively, such as electron beam computed tomography, have revolutionized our current thinking about the risks of vascular calcification. In coronary arteries, calcification is positively correlated with atherosclerotic plaque burden (11,12), increased risk of myocardial infarction (13)(14)(15), and plaque instability (2,16). Although some of these findings may relate to the correlation of coronary calcification with extent of underlying atherosclerotic disease, it is also possible that vascular calcification itself may contribute to initiation or progression of cardiovascular disease (CVD).…”

Section: Clinical Consequences Of Vascular Calcificationmentioning

confidence: 99%

Vascular Calcification Mechanisms

Giachelli

2004

Journal of the American Society of Nephrology

484

396

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Section: Clinical Consequences Of Vascular Calcificationmentioning

confidence: 99%

Vascular Calcification Mechanisms

Giachelli

2004

Journal of the American Society of Nephrology

484

396

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“…Fitzgerald and colleagues demonstrated a strong correlation between calcification and dissection after balloon angioplasty. 163 In this light, it is important to consider that plaque stability in zones of calcification may also be related to MMP activity and matrix remodeling, which are known to reduce lesion stability in the shoulder regions. Further investigations are required to precisely define the role of calcification in plaque stability, which will hopefully include more detailed analyses of the activities of proteolytic enzymes as well as the collagen metabolism in these discrete regions of advanced lesions.…”

Section: Atherosclerotic Calcificationmentioning

confidence: 99%

Collagens in the progression and complications of atherosclerosis

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.

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“…Atherosclerotic calcification of coronary artery is a significant risk for the unsuccessful coronary intervention and balloon-induced coronary artery dissection (1), and calcification is found to be an indicator of plaque instability (2). Although inhibition of atherosclerotic calcification might be a promising approach to stabilize atherosclerotic plaques, the molecular mechanism(s) underlying atherosclerotic vascular calcification remains incompletely understood.…”

mentioning

confidence: 99%

Oxidized Low Density Lipoprotein Induces Bone Morphogenetic Protein-2 in Coronary Artery Endothelial Cells via Toll-like Receptors 2 and 4

Shi

et al. 2011

Journal of Biological Chemistry

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Vascular calcification is a common complication in atherosclerosis. Bone morphogenetic protein-2 (BMP-2) plays an important role in atherosclerotic vascular calcification. The aim of this study was to determine the effect of oxidized low density lipoprotein (oxLDL) on BMP-2 protein expression in human coronary artery endothelial cells (CAECs), the roles of Toll-like receptor (TLR) 2 and TLR4 in oxLDL-induced BMP-2 expression, and the signaling pathways involved. Human CAECs were stimulated with oxLDL. The roles of TLR2 and TLR4 in oxLDLinduced BMP-2 expression were determined by pretreatment with neutralizing antibody, siRNA, and overexpression. Stimulation with oxLDL increased cellular BMP-2 protein levels in a dose-dependent manner (40 -160 g/ml). Pretreatment with neutralizing antibodies against TLR2 and TLR4 or silencing of these two receptors reduced oxLDL-induced BMP-2 expression. Overexpression of TLR2 and TLR4 enhanced the cellular BMP-2 response to oxLDL. Furthermore, oxLDL was co-localized with TLR2 and TLR4. BMP-2 expression was associated with activation of nuclear factor-B (NF-B), p38 mitogen-activated protein kinase (MAPK), and extracellular signal-regulated kinase (ERK)1/2. Inhibition of NF-B and ERK1/2 reduced BMP-2 expression whereas inhibition of p38 MAPK had no effect. In conclusion, oxLDL induces BMP-2 expression through TLR2 and TLR4 in human CAECs. The NF-B and ERK1/2 pathways are involved in the signaling mechanism. These findings underscore an important role for TLR2 and TLR4 in mediating the BMP-2 response to oxLDL in human CAECs and indicate that these two immunoreceptors contribute to the mechanisms underlying atherosclerotic vascular calcification.Calcification in intima is often associated with atherosclerosis. Atherosclerotic calcification of coronary artery is a significant risk for the unsuccessful coronary intervention and balloon-induced coronary artery dissection (1), and calcification is found to be an indicator of plaque instability (2). Although inhibition of atherosclerotic calcification might be a promising approach to stabilize atherosclerotic plaques, the molecular mechanism(s) underlying atherosclerotic vascular calcification remains incompletely understood.It is known that oxLDL 2 accumulation in the vascular wall provokes the development of atherosclerosis and vascular calcification (3). BMP-2 is an osteogenic factor. It is expressed in calcified human atherosclerotic plaque. Cells from the atherogenic aortic wall express BMP-2 in vitro and formed calcified nodules with prolonged culture (4). The BMP-2 mRNA level increased after oxLDL stimulation in human CAECs (5). However, it remains unclear whether oxLDL up-regulates BMP-2 protein levels in CAECs. Further, the signaling mechanism that regulates the cellular BMP-2 response to oxLDL is unknown.Accumulating evidence indicates that atherosclerosis is an inflammatory process involving a network of vascular cells, monocytes, and T lymphocytes. Proinflammatory mediators, including cytokines, chemokines, and growth factors...

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Contribution of localized calcium deposits to dissection after angioplasty. An observational study using intravascular ultrasound.

Cited by 478 publications

References 24 publications

Vascular Calcification Mechanisms

Vascular Calcification Mechanisms

Collagens in the progression and complications of atherosclerosis

Oxidized Low Density Lipoprotein Induces Bone Morphogenetic Protein-2 in Coronary Artery Endothelial Cells via Toll-like Receptors 2 and 4

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