&lt;i&gt;CDKN2B&lt;/i&gt; Methylation and Aortic Arch Calcification in Patients with Ischemic Stroke

Zhou, Shuyu; Cai, Biyang; Zhang, Zhizhong; Zhang, Yumeng; Wang, Li; Liu, Keting; Zhang, Hao; Sun, Lingli; Cai, Huan; Lu, Guangming; Liu, Xinfeng; Xu, Gelin

doi:10.5551/jat.36897

Cited by 22 publications

(19 citation statements)

References 37 publications

(46 reference statements)

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“…In addition, it is known that vascular calcification affects intracellular signaling, due to epigenetic phenomena, including altered microRNA levels, DNA methylation, and histone modifications. In addition, aging affects calcification through osteoinductive signaling, inflammatory cytokines, and oxidative stress [78,[81][82][83][84][85]. Moreover, cellular phenomena that affect osteoinductive intracellular signaling, via hyperphosphatemia, include autophagy, ER stress, and mitochondrial dysfunction.…”

Section: Vascular Smooth Muscle Cell Phenotypic Differentiation In Himentioning

confidence: 99%

Vascular Calcification—New Insights into Its Mechanism

Lee

Jeon

2020

IJMS

237

254

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Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

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Section: Vascular Smooth Muscle Cell Phenotypic Differentiation In Himentioning

confidence: 99%

Vascular Calcification—New Insights into Its Mechanism

Lee

Jeon

2020

IJMS

237

254

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“…Higher level of DNA methylation of cyclin dependent kinase inhibitor 2B (CDKN2B), a gene involved in the pathogenesis of both atherosclerosis and arterial calcification, was associated with increased susceptibility to calcification of the arteries in patients with IS [58].…”

Section: Dna Methylation In Ismentioning

confidence: 99%

“…The hypomethylation of TNF receptor-associated factor 3 (TRAF3) and of protein phosphatase 1A (PPM1A) is also related to increased stroke occurrence in patients treated with antiplatelet drugs [62,63]. Aortic arch calcification [58] Elderly patients Hypomethylation of LINE-1 levels of VCAM-1 in elderly individuals. In the same study, the authors reported that the association between LINE-1 hypomethylation and VCAM-1 expression was significant only in subjects without prevalent ischemic heart disease or stroke.…”

Section: Study Model Condition/effects Outcomes Referencesmentioning

confidence: 99%

“…The hypomethylation of TNF receptor-associated factor 3 (TRAF3) and atase 1A (PPM1A) is also related to increased stroke occurrence in patients treated rugs [62,63]. ⬆Aortic arch calcification [58] indicates decrease whereas Vascular cell adhesion protein 1 level (VCAM-1) represents a marker of cardiovascular diseases since it is rapidly expressed in pro-atherosclerotic conditions [59,60]. Baccarelli et al showed that the hypomethylation of long interspersed nucleotide elements (LINE-1) was associated with increased levels of VCAM-1 in elderly individuals.…”

Section: Study Model Condition/effects Outcomes Referencesmentioning

confidence: 99%

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Pathogenesis of Ischemic Stroke: Role of Epigenetic Mechanisms

Stanzione

Cotugno

Bianchi

et al. 2020

Genes

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Epigenetics is the branch of molecular biology that studies modifications able to change gene expression without altering the DNA sequence. Epigenetic modulations include DNA methylation, histone modifications, and noncoding RNAs. These gene modifications are heritable and modifiable and can be triggered by lifestyle and nutritional factors. In recent years, epigenetic changes have been associated with the pathogenesis of several diseases such as diabetes, obesity, renal pathology, and different types of cancer. They have also been related with the pathogenesis of cardiovascular diseases including ischemic stroke. Importantly, since epigenetic modifications are reversible processes they could assist with the development of new therapeutic approaches for the treatment of human diseases. In the present review article, we aim to collect the most recent evidence concerning the impact of epigenetic modifications on the pathogenesis of ischemic stroke in both animal models and humans.

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“…Interestingly, most reports (n = 40; 60.6%) looked into the pathogenic role of non-coding RNA in VC, while histone modification (n = 6; 9.1%) [53][54][55][56][57][58], DNA methylation (n = 8; 12.1%) [5,[59][60][61][62][63][64][65], and chromatin changes (n = 3; 4.5%) [66][67][68] accounted for one-fourth only. Nine (13.6%) [69][70][71][72][73][74][75][76][77] examined the discrepancy of epigenetic signatures between subjects or animals with and without VC but not their pathogenic influences. In the following sections, we summarize results from these reports and try to synthesize an inter-connected network of epigenetic regulation of VC based on the existing data assisted by bioinformatic integration.…”

Section: Strategy Of Literature Review and Findingsmentioning

confidence: 99%

The Epigenetic Landscape of Vascular Calcification: An Integrative Perspective

Hou

Yuan

et al. 2020

IJMS

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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.

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<i>CDKN2B</i> Methylation and Aortic Arch Calcification in Patients with Ischemic Stroke

Cited by 22 publications

References 37 publications

Vascular Calcification—New Insights into Its Mechanism

Vascular Calcification—New Insights into Its Mechanism

Pathogenesis of Ischemic Stroke: Role of Epigenetic Mechanisms

The Epigenetic Landscape of Vascular Calcification: An Integrative Perspective

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