The Epigenetic Landscape of Vascular Calcification: An Integrative Perspective

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 u...

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Published inInternational journal of molecular sciences Vol. 21; no. 3; p. 980
Main Authors Hou, Yi-Chou, Lu, Chien-Lin, Yuan, Tzu-Hang, Liao, Min-Tser, Chao, Chia-Ter, Lu, Kuo-Cheng
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.02.2020
MDPI
Subjects
Calcification
DNA methylation
Epigenetics
Growth factors
Kinases
MicroRNAs
Pathogenesis
Review
Smooth muscle
Transcription factors
chronic kidney disease
epigenetic
vascular calcification
phosphate
microRNA
diabetes mellitus
medial calcification
vascular smooth muscle cells
Online AccessGet full text
ISSN1422-0067
1661-6596
1422-0067
DOI10.3390/ijms21030980

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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.
AbstractList 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.
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.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.
Author Yuan, Tzu-Hang
Lu, Kuo-Cheng
Chao, Chia-Ter
Hou, Yi-Chou
Liao, Min-Tser
Lu, Chien-Lin
AuthorAffiliation 8 Department of Internal Medicine, National Taiwan University Hospital BeiHu Branch, Taipei 108, Taiwan
1 Division of Nephrology, Department of Medicine, Cardinal-Tien Hospital, School of Medicine, Fu-Jen Catholic University, New Taipei City 234, Taiwan; athletics910@gmail.com
2 Division of Nephrology, Department of Medicine, Fu-Jen Catholic University Hospital, School of Medicine, Fu-Jen Catholic University, New Taipei City 243, Taiwan; janlin0123@gmail.com (C.-L.L.); kuochenglu@gmail.com (K.-C.L.)
4 Department of Pediatrics, Taoyuan Armed Forces General Hospital, Taoyuan City 325, Taiwan; liaoped804h@yahoo.com.tw
6 Department of Pediatrics, Fu-Jen Catholic University Hospital, School of Medicine, Fu-Jen Catholic University, New Taipei City 243, Taiwan
5 Department of Pediatrics, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
7 Nephrology division, Department of Internal Medicine, National Taiwan University Hospital, Taipei 100, Taiwan
3 Graduate Institute
AuthorAffiliation_xml – name: 3 Graduate Institute of Toxicology, National Taiwan University College of Medicine, Taipei 104, Taiwan; yuan.tzu.h@gmail.com
– name: 4 Department of Pediatrics, Taoyuan Armed Forces General Hospital, Taoyuan City 325, Taiwan; liaoped804h@yahoo.com.tw
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– name: 8 Department of Internal Medicine, National Taiwan University Hospital BeiHu Branch, Taipei 108, Taiwan
– name: 2 Division of Nephrology, Department of Medicine, Fu-Jen Catholic University Hospital, School of Medicine, Fu-Jen Catholic University, New Taipei City 243, Taiwan; janlin0123@gmail.com (C.-L.L.); kuochenglu@gmail.com (K.-C.L.)
– name: 6 Department of Pediatrics, Fu-Jen Catholic University Hospital, School of Medicine, Fu-Jen Catholic University, New Taipei City 243, Taiwan
– name: 1 Division of Nephrology, Department of Medicine, Cardinal-Tien Hospital, School of Medicine, Fu-Jen Catholic University, New Taipei City 234, Taiwan; athletics910@gmail.com
– name: 5 Department of Pediatrics, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan
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Keywords chronic kidney disease
epigenetic
vascular calcification
phosphate
microRNA
diabetes mellitus
medial calcification
vascular smooth muscle cells
Language English
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Snippet Vascular calcification (VC) is an important complication among patients of advanced age, those with chronic kidney disease, and those with diabetes mellitus....
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SubjectTerms Calcification
DNA methylation
Epigenetics
Growth factors
Kinases
MicroRNAs
Pathogenesis
Review
Smooth muscle
Transcription factors
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Title The Epigenetic Landscape of Vascular Calcification: An Integrative Perspective
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