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  4. The epigenetic landscape of vascular calcification: An integrative perspective
 
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The epigenetic landscape of vascular calcification: An integrative perspective

Journal
International Journal of Molecular Sciences
Journal Volume
21
Journal Issue
3
Pages
980
Date Issued
2020
Author(s)
Hou Y.-C.
Lu C.-L.
Yuan T.-H.
Liao M.-T.
CHIA-TER CHAO  
Lu K.-C.
DOI
10.3390/ijms21030980
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85079062207&doi=10.3390%2fijms21030980&partnerID=40&md5=cdf55049c422be2abeef66393eee128e
https://scholars.lib.ntu.edu.tw/handle/123456789/578705
Abstract
Vascular calcification (VC) is an important complication among patients of advanced age, those with chronic kidney disease, and those with diabetes mellitus. The pathophysiology of VC encompasses passive occurrence of physico-chemical calcium deposition, active cellular secretion of osteoid matrix upon exposure to metabolically noxious stimuli, or a variable combination of both processes. Epigenetic alterations have been shown to participate in this complex environment, through mechanisms including DNA methylation, non-coding RNAs, histone modifications, and chromatin changes. Despite such importance, existing reviews fail to provide a comprehensive view of all relevant reports addressing epigenetic processes in VC, and cross-talk between different epigenetic machineries is rarely examined. We conducted a systematic review based on PUBMED and MEDLINE databases up to 30 September 2019, to identify clinical, translational, and experimental reports addressing epigenetic processes in VC; we retrieved 66 original studies, among which 60.6% looked into the pathogenic role of non-coding RNA, followed by DNA methylation (12.1%), histone modification (9.1%), and chromatin changes (4.5%). Nine (13.6%) reports examined the discrepancy of epigenetic signatures between subjects or tissues with and without VC, supporting their applicability as biomarkers. Assisted by bioinformatic analyses blending in each epigenetic component, we discovered prominent interactions between microRNAs, DNA methylation, and histone modification regarding potential influences on VC risk. ? 2020 by the authors. Licensee MDPI, Basel, Switzerland.
Subjects
Chronic kidney disease; Diabetes mellitus; Epigenetic; Medial calcification; MicroRNA; Phosphate; Vascular calcification; Vascular smooth muscle cells
SDGs

[SDGs]SDG3

Other Subjects
alkaline phosphatase; beta catenin; biological marker; histone methyltransferase; interleukin 6; kruppel like factor 4; long untranslated RNA; microRNA; microRNA 125b; microRNA 133a; microRNA 143; microRNA 155; microRNA 182; microRNA 204; microRNA 205; microRNA 21; microRNA 222; microRNA 26a; microRNA 302b; microRNA 30b; microRNA 32; microRNA 762; nitric oxide; osteocalcin; peptides and proteins; protein p53; reactive oxygen metabolite; stress activated protein kinase; transcription factor RUNX2; unclassified drug; unindexed drug; adipogenesis; angiogenesis; apoptosis; atherosclerosis; bioinformatics; blood vessel calcification; cell differentiation; chromatin; cytokine release; DNA methylation; down regulation; epigenetic repression; gene control; gene expression; histone acetylation; histone modification; homologous recombination; human; microarray analysis; nonhuman; nucleosome; oxidative stress; pathogenesis; pathophysiology; promoter region; real time polymerase chain reaction; Review; systematic review; tumor suppressor gene; ubiquitination; vascular smooth muscle cell; animal; blood vessel calcification; DNA methylation; gene expression regulation; genetic epigenesis; genetics; Animals; DNA Methylation; Epigenesis, Genetic; Gene Expression Regulation; Humans; Vascular Calcification
Publisher
MDPI AG
Type
review

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