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      Role of Inflammation in Arterial Calcification

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          • Arterial calcification can be divided into intimal calcification and medial calcification which have strong correlations with adverse cardiovascular events. Continuous research on vascular calcification has been performed, and several cellular and molecular mechanisms and therapeutic targets were identified. However, despite clinical trials to evaluate the efficacy of drug therapies to treat vascular calcification, none have been shown to have efficacy until the present. Therefore, more extensive research is necessary to develop appropriate therapeutic strategies based on a thorough understanding of vascular calcification. In this review, we mainly focus on the pathobiology of arterial calcification, and its clinical implications.

          Abstract

          Arterial calcification, characterized by calcium phosphate deposition in the arteries, can be divided into intimal calcification and medial calcification. The former is the predominant form of calcification in coronary artery plaques; the latter mostly affects peripheral arteries and aortas. Both forms of arterial calcification have strong correlations with adverse cardiovascular events. Intimal microcalcification is associated with increased risk of plaque disruption while the degree of burden of coronary calcification, measured by coronary calcium score, is a marker of overall plaque burden. Continuous research on vascular calcification has been performed during the past few decades, and several cellular and molecular mechanisms and therapeutic targets were identified. However, despite clinical trials to evaluate the efficacy of drug therapies to treat vascular calcification, none have been shown to have efficacy until the present. Therefore, more extensive research is necessary to develop appropriate therapeutic strategies based on a thorough understanding of vascular calcification. In this review, we mainly focus on intimal calcification, namely the pathobiology of arterial calcification, and its clinical implications.

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          Most cited references83

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          Coronary calcium as a predictor of coronary events in four racial or ethnic groups.

          In white populations, computed tomographic measurements of coronary-artery calcium predict coronary heart disease independently of traditional coronary risk factors. However, it is not known whether coronary-artery calcium predicts coronary heart disease in other racial or ethnic groups. We collected data on risk factors and performed scanning for coronary calcium in a population-based sample of 6722 men and women, of whom 38.6% were white, 27.6% were black, 21.9% were Hispanic, and 11.9% were Chinese. The study subjects had no clinical cardiovascular disease at entry and were followed for a median of 3.8 years. There were 162 coronary events, of which 89 were major events (myocardial infarction or death from coronary heart disease). In comparison with participants with no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among participants with coronary calcium scores between 101 and 300 and by a factor of 9.67 among participants with scores above 300 (P<0.001 for both comparisons). Among the four racial and ethnic groups, a doubling of the calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary event by 18 to 39%. The areas under the receiver-operating-characteristic curves for the prediction of both major coronary events and any coronary event were higher when the calcium score was added to the standard risk factors. The coronary calcium score is a strong predictor of incident coronary heart disease and provides predictive information beyond that provided by standard risk factors in four major racial and ethnic groups in the United States. No major differences among racial and ethnic groups in the predictive value of calcium scores were detected. Copyright 2008 Massachusetts Medical Society.
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            Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

            Abstract 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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              Interleukin-1 Beta as a Target for Atherosclerosis Therapy: Biological Basis of CANTOS and Beyond.

              Inflammatory pathways drive atherogenesis and link conventional risk factors to atherosclerosis and its complications. One inflammatory mediator has come to the fore as a therapeutic target in cardiovascular disease. The experimental and clinical evidence reviewed here support interleukin-1 beta (IL-1β) as both a local vascular and systemic contributor in this regard. Intrinsic vascular wall cells and lesional leukocytes alike can produce this cytokine. Local stimuli in the plaque favor the generation of active IL-1β through the action of a molecular assembly known as the inflammasome. Clinically applicable interventions that interfere with IL-1 action can improve cardiovascular outcomes, ushering in a new era of anti-inflammatory therapies for atherosclerosis. The translational path described here illustrates how advances in basic vascular biology may transform therapy. Biomarker-directed application of anti-inflammatory interventions promises to help us achieve a more precise and personalized allocation of therapy for our cardiovascular patients.
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                Author and article information

                Journal
                Korean Circ J
                Korean Circ J
                KCJ
                Korean Circulation Journal
                The Korean Society of Cardiology
                1738-5520
                1738-5555
                February 2021
                25 January 2021
                : 51
                : 2
                : 114-125
                Affiliations
                [1 ]Department of Internal Medicine and Cardiovascular Center, Seoul National University Hospital, Seoul, Korea.
                [2 ]Institute for Bio-Medical Convergence, College of Medicine, Catholic Kwandong University, Gangneung, Korea.
                [3 ]Division of Cardiology, Severance Cardiovascular Hospital and Integrative Research Center for Cerebrovascular and Cardiovascular Diseases, Yonsei University College of Medicine,, Seoul, Korea.
                Author notes
                Correspondence to Sungha Park, MD, PhD. Division of Cardiology, Severance Cardiovascular Hospital and Integrative Research Center for Cerebrovascular and Cardiovascular Diseases, Yonsei University College of Medicine, Seoul 03722, Korea. shpark0530@ 123456yuhs.ac

                *Hae-Young Lee and Soyeon Lim contributed equally.

                Author information
                https://orcid.org/0000-0002-9521-4102
                https://orcid.org/0000-0001-9814-0682
                https://orcid.org/0000-0001-5362-478X
                Article
                10.4070/kcj.2020.0517
                7853899
                33525066
                7837be11-0c00-4867-9edb-e70a5c839a4f
                Copyright © 2021. The Korean Society of Cardiology

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( https://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 December 2020
                : 24 December 2020
                Funding
                Funded by: National Research Foundation of Korea, CrossRef https://doi.org/10.13039/501100003725;
                Award ID: NRF-2020R1A2C1007103
                Award ID: 2018R1A1A1A05078230
                Categories
                State of the Art Review

                Cardiovascular Medicine
                arterial calcification,pathobiology,therapeutic strategy,clinical implication

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