The predictive value of arterial and valvular calcification for mortality and cardiovascular events

Nicoll, Rachel; Henein, Michael Y.

doi:10.1016/j.ijchv.2014.02.001

Cited by 39 publications

(32 citation statements)

References 79 publications

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“…Vascular calcification, the deposition of hydroxyapatite mineral in the arterial wall, is linked to an increased risk of heart disease, stroke, atherosclerotic plaque rupture. 1 Calcification occurs in both the intimal and medial layers of the arteries. Intimal calcification is linked to arterial obstruction and atherosclerotic plaque rupture.…”

Section: Introductionmentioning

confidence: 99%

Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

Durham

Speer

Scatena

et al. 2018

Cardiovascular Research

768

662

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Vascular calcification is associated with a significant increase in all-cause mortality and atherosclerotic plaque rupture. Calcification has been determined to be an active process driven in part by vascular smooth muscle cell (VSMC) transdifferentiation within the vascular wall. Historically, VSMC phenotype switching has been viewed as binary, with the cells able to adopt a physiological contractile phenotype or an alternate ‘synthetic’ phenotype in response to injury. More recent work, including lineage tracing has however revealed that VSMCs are able to adopt a number of phenotypes, including calcific (osteogenic, chondrocytic, and osteoclastic), adipogenic, and macrophagic phenotypes. Whilst the mechanisms that drive VSMC differentiation are still being elucidated it is becoming clear that medial calcification may differ in several ways from the intimal calcification seen in atherosclerotic lesions, including risk factors and specific drivers for VSMC phenotype changes and calcification. This article aims to compare and contrast the role of VSMCs in driving calcification in both atherosclerosis and in the vessel media focusing on the major drivers of calcification, including aging, uraemia, mechanical stress, oxidative stress, and inflammation. The review also discusses novel findings that have also brought attention to specific pro- and anti-calcifying proteins, extracellular vesicles, mitochondrial dysfunction, and a uraemic milieu as major determinants of vascular calcification.

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Section: Introductionmentioning

confidence: 99%

Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

Durham

Speer

Scatena

et al. 2018

Cardiovascular Research

768

662

View full text Add to dashboard Cite

show abstract

“…In abnormal circumstances, hydroxyapatite, a calcium phosphate mineral, can be deposited in blood vessels, which is linked to aging and cardiovascular or metabolic diseases such as atherosclerosis, chronic kidney disease, and diabetes. 1 This phenomenon, called vascular calcification, causes remodeling of the blood vessels, resulting in an increase in stiffness. Because this abnormal rigidity itself can cause secondary fatal diseases such as ischemia of distal tissue or rupture, vascular calcification is often considered an independent risk factor for cardiovascular events.…”

Section: Introductionmentioning

confidence: 99%

miR-27a-3p Targets ATF3 to Reduce Calcium Deposition in Vascular Smooth Muscle Cells

Choe

Kwon

Ryu

et al. 2020

Molecular Therapy - Nucleic Acids

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Vascular calcification, the ectopic deposition of calcium in blood vessels, develops in association with various metabolic diseases and atherosclerosis and is an independent predictor of morbidity and mortality associated with these diseases. Herein, we report that reduction of microRNA-27a-3p ( miR-27a-3p ) causes an increase in activating transcription factor 3 (ATF3), a novel osteogenic transcription factor, in vascular smooth muscle cells. Both microRNA (miRNA) and mRNA microarrays were performed with rat vascular smooth muscle cells, and reciprocally regulated pairs of miRNA and mRNA were selected after bioinformatics analysis. Inorganic phosphate significantly reduced the expression of miR-27a-3p in A10 cells. The transcript level was also reduced in vitamin D 3 -administered mouse aortas. miR-27a-3p mimic reduced calcium deposition, whereas miR-27a-3p inhibitor increased it. The Atf3 mRNA level was upregulated in a cellular vascular calcification model, and miR-27a-3p reduced the Atf3 mRNA and protein levels. Transfection with Atf3 could recover the miR-27a-3p -induced reduction of calcium deposition. Our results suggest that reduction of miR-27a-3p may contribute to the development of vascular calcification by de-repression of ATF3.

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“…In vascular calcification, which is the final step in the development of atherosclerosis, the deposition of hydroxyapatite mineral in the arterial wall has been associated with an increased risk of heart disease, stroke, and atherosclerotic plaque rupture [ 14 ]. However, there is only limited information available on the association between periodontal diseases and carotid artery calcification (CAC).…”

Section: Introductionmentioning

confidence: 99%

Association between Carotid Artery Calcification and Periodontal Disease Progression in Japanese Men and Women: A Cross-Sectional Study

Dewake

Ishioka

Uchida

et al. 2020

JCM

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Objective: To evaluate the association between alveolar bone loss (ABL) detected on panoramic radiographs and carotid artery calcification (CAC) detected on computed tomography (CT). Methods: The study subjects included 295 patients (mean age ± SD: 64.6 ± 11.8 years) who visited the Matsumoto Dental University Hospital. The rate of ABL and the number of present teeth were measured on panoramic radiographs. Univariate analyses with t-tests and chi-squared tests were performed to evaluate the differences in age, gender, history of diseases, number of present teeth, and the ABL between subjects, with and without CAC. Moreover, multivariate logistic regression analysis, with forward selection and receiver operating characteristic curve (ROC) analysis, was performed. Results: The number of subjects without and with CAC was 174 and 121, respectively. Univariate analyses revealed that CAC was significantly associated with age, hypertension, osteoporosis, number of present teeth, and ABL. Multivariate logistic regression analysis adjusted for covariates revealed that the presence of CAC was significantly associated with ABL (OR = 1.233, 95% CI = 1.167–1.303). In the ROC analysis for predicting the presence of CAC, the the area under the ROC curve was the highest at 0.932 (95% CI = 0.904–0.960) for ABL, which was significant. Conclusions: Our results suggest that the measurement of ABL on panoramic radiographs may be an effective approach to identifying patients with an increased risk of CAC.

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The predictive value of arterial and valvular calcification for mortality and cardiovascular events

Cited by 39 publications

References 79 publications

Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

miR-27a-3p Targets ATF3 to Reduce Calcium Deposition in Vascular Smooth Muscle Cells

Association between Carotid Artery Calcification and Periodontal Disease Progression in Japanese Men and Women: A Cross-Sectional Study

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