598 487

Cited 38 times in

Cited 36 times in

Role of Inflammation in Arterial Calcification

DC Field Value Language
dc.contributor.authorLee, Hae Young-
dc.contributor.authorLim, Soyeon-
dc.contributor.authorPark, Sungha-
dc.date.accessioned2021-04-29T17:00:23Z-
dc.date.available2021-04-29T17:00:23Z-
dc.date.created2021-08-25-
dc.date.issued2021-02-
dc.identifier.issn1738-5520-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/182133-
dc.description.abstractArterial 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.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish, Korean-
dc.publisherKorean Society of Circulation-
dc.relation.isPartOfKOREAN CIRCULATION JOURNAL-
dc.relation.isPartOfKOREAN CIRCULATION JOURNAL-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleRole of Inflammation in Arterial Calcification-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학교실)-
dc.contributor.googleauthorLee, Hae Young-
dc.contributor.googleauthorLim, Soyeon-
dc.contributor.googleauthorPark, Sungha-
dc.identifier.doi10.4070/kcj.2020.0517-
dc.relation.journalcodeJ01952-
dc.identifier.eissn1738-5555-
dc.subject.keywordArterial calcification-
dc.subject.keywordPathobiology-
dc.subject.keywordTherapeutic strategy-
dc.subject.keywordClinical implication-
dc.contributor.alternativeNamePark, Sung Ha-
dc.contributor.affiliatedAuthorPark, Sungha-
dc.identifier.scopusid2-s2.0-85101271630-
dc.identifier.wosid000624292500002-
dc.citation.volume51-
dc.citation.number2-
dc.citation.startPage114-
dc.citation.endPage125-
dc.identifier.bibliographicCitationKOREAN CIRCULATION JOURNAL, Vol.51(2) : 114-125, 2021-02-
dc.identifier.rimsid71300-
dc.type.rimsART-
dc.description.journalClass1-
dc.description.journalClass1-
dc.subject.keywordAuthorArterial calcification-
dc.subject.keywordAuthorPathobiology-
dc.subject.keywordAuthorTherapeutic strategy-
dc.subject.keywordAuthorClinical implication-
dc.subject.keywordPlusENDOTHELIAL-MESENCHYMAL TRANSITION-
dc.subject.keywordPlusACUTE MYOCARDIAL-INFARCTION-
dc.subject.keywordPlusNECROSIS-FACTOR-ALPHA-
dc.subject.keywordPlusSMOOTH-MUSCLE-CELLS-
dc.subject.keywordPlusVASCULAR CALCIFICATION-
dc.subject.keywordPlusCORONARY CALCIFICATION-
dc.subject.keywordPlusALKALINE-PHOSPHATASE-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusSTATIN THERAPY-
dc.subject.keywordPlusATHEROSCLEROSIS-
dc.type.docTypeReview-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalWebOfScienceCategoryCardiac & Cardiovascular Systems-
dc.relation.journalResearchAreaCardiovascular System & Cardiology-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.