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      Bibliometric and Visual Analysis of Vascular Calcification Research

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          Abstract

          Background: Extensive studies related to vascular calcification (VC) were conducted in recent years. However, no bibliometric analysis has systematically investigated this topic. Our study aimed to determine the hotspots and frontiers of VC research in the past decade and provide a reference for future scientific research directions and decision-making in the VC field.

          Methods: VC studies were acquired from the Web of Science Core Collection. Bibliometric and visual analyses were performed using CiteSpace, VOSviewer, and Microsoft Excel software.

          Results: A total of 8,238 English articles on VC research published in 2011–2020 were obtained. In the past decade, annual publications and citations showed a significant growth trend, especially in 2018–2020. The most productive country, institution, journal and author are the United States, the University of California System, PLOS ONE, and Budoff MJ, respectively. The most frequently cited country, journal, and author are the United States, Journal of the American College of Cardiology, and Floege J, respectively. “Vascular calcification,” “atherosclerosis,” “chronic kidney disease,” and “cardiovascular disease” are the primary keywords. The burst keywords “revascularization,” “calciprotein particle,” “microRNA,” and “microcalcification” are speculated to be the research frontiers.

          Conclusion: The main research hotspots in the VC field are the molecular mechanisms and prognosis of VC in patients with chronic kidney disease or cardiovascular disease. In addition, endovascular therapy and the development of new drugs targeting signal pathways for VC will become the focus of future research. Moreover, non-coding RNAs related to the diagnosis and treatment of VC are great research prospects.

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          Most cited references56

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          Software survey: VOSviewer, a computer program for bibliometric mapping

          We present VOSviewer, a freely available computer program that we have developed for constructing and viewing bibliometric maps. Unlike most computer programs that are used for bibliometric mapping, VOSviewer pays special attention to the graphical representation of bibliometric maps. The functionality of VOSviewer is especially useful for displaying large bibliometric maps in an easy-to-interpret way. The paper consists of three parts. In the first part, an overview of VOSviewer’s functionality for displaying bibliometric maps is provided. In the second part, the technical implementation of specific parts of the program is discussed. Finally, in the third part, VOSviewer’s ability to handle large maps is demonstrated by using the program to construct and display a co-citation map of 5,000 major scientific journals.
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            CiteSpace II: Detecting and visualizing emerging trends and transient patterns in scientific literature

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              Mechanisms of plaque formation and rupture.

              Atherosclerosis causes clinical disease through luminal narrowing or by precipitating thrombi that obstruct blood flow to the heart (coronary heart disease), brain (ischemic stroke), or lower extremities (peripheral vascular disease). The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and calcification. After decades of indolent progression, such plaques may suddenly cause life-threatening coronary thrombosis presenting as an acute coronary syndrome. Most often, the culprit morphology is plaque rupture with exposure of highly thrombogenic, red cell-rich necrotic core material. The permissive structural requirement for this to occur is an extremely thin fibrous cap, and thus, ruptures occur mainly among lesions defined as thin-cap fibroatheromas. Also common are thrombi forming on lesions without rupture (plaque erosion), most often on pathological intimal thickening or fibroatheromas. However, the mechanisms involved in plaque erosion remain largely unknown, although coronary spasm is suspected. The calcified nodule has been suggested as a rare cause of coronary thrombosis in highly calcified and tortious arteries in older individuals. To characterize the severity and prognosis of plaques, several terms are used. Plaque burden denotes the extent of disease, whereas plaque activity is an ambiguous term, which may refer to one of several processes that characterize progression. Plaque vulnerability describes the short-term risk of precipitating symptomatic thrombosis. In this review, we discuss mechanisms of atherosclerotic plaque initiation and progression; how plaques suddenly precipitate life-threatening thrombi; and the concepts of plaque burden, activity, and vulnerability. © 2014 American Heart Association, Inc.
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                Author and article information

                Contributors
                Journal
                Front Pharmacol
                Front Pharmacol
                Front. Pharmacol.
                Frontiers in Pharmacology
                Frontiers Media S.A.
                1663-9812
                15 July 2021
                2021
                : 12
                : 690392
                Affiliations
                [ 1 ]Department of Anesthesiology, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China
                [ 2 ]Department of Anesthesiology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China
                [ 3 ]Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China
                Author notes

                Edited by: Tim David Hewitson, Royal Melbourne Hospital, Australia

                Reviewed by: Dejian Yu, Nanjing Audit University, China

                Belinda Di Bartolo, The University of Sydney, Australia

                *Correspondence: Xiongqing Huang, huangxq@ 123456mail.sysu.edu.cn ; Qin Zhou, zhouqin5@ 123456mail.sysu.edu.cn
                [†]

                These authors have contributed equally to this work and share first authorship

                This article was submitted to Cardiovascular and Smooth Muscle Pharmacology, a section of the journal Frontiers in Pharmacology

                Article
                690392
                10.3389/fphar.2021.690392
                8319769
                34335257
                584a54c9-10ad-4f05-b700-b9b5e9475640
                Copyright © 2021 Dong, Liang, Chen, Li, Lu, Huang and Zhou.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 02 April 2021
                : 05 July 2021
                Funding
                Funded by: National Science Foundation 10.13039/100000001
                Categories
                Pharmacology
                Original Research

                Pharmacology & Pharmaceutical medicine
                vascular calcification1,chronic kidney disease2,atherosclerosis3,vascular smooth muscle cell4,citespace5,vosviewer6,bibliometrics7

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