DNA modifications in atherosclerosis: From the past to the future

Borghini, Andrea; Cervelli, Tiziana; Galli, Alvaro; Andreassi, Maria Grazia

doi:10.1016/j.atherosclerosis.2013.07.038

Cited by 48 publications

(26 citation statements)

References 78 publications

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“…Many studies report the contribution of miRNAs in the pathogenesis of atherosclerosis, demonstrating their role in endothelial integrity, SMC proliferation, cholesterol synthesis, lipid metabolism, and inflammatory response to oxidized LDL (oxLDL) [12]. More recently, many lncRNAs have been involved in cell differentiation, cell cycle, and the maintenance of stem-cell-like phenotypes.…”

Section: Atherosclerosis and Epigenetic Modificationsmentioning

confidence: 99%

Epigenetic Reprogramming in Atherosclerosis

Grimaldi

Vietri

Schiano

et al. 2014

Curr Atheroscler Rep

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Recent data support the involvement of epigenetic alterations in the pathogenesis of atherosclerosis. The most widely investigated epigenetic mechanism is DNA methylation although also histone code changes occur during the diverse steps of atherosclerosis, such as endothelial cell proliferation, vascular smooth muscle cell (SMC) differentiation, and inflammatory pathway activation. In this review, we focus on the main genes that are epigenetically modified during the atherogenic process, particularly nitric oxide synthase (NOS), estrogen receptors (ERs), collagen type XV alpha 1 (COL15A1), vascular endothelial growth factor receptor (VEGFR), and ten-eleven translocation (TET), which are involved in endothelial dysfunction; gamma interferon (IFN-γ), forkhead box p3 (FOXP3), and tumor necrosis factor-α (TNF-α), associated with atherosclerotic inflammatory process; and p66shc, lectin-like oxLDL receptor (LOX1), and apolipoprotein E (APOE) genes, which are regulated by high cholesterol and homocysteine (Hcy) levels. Furthermore, we also discuss the role of non-coding RNAs (ncRNA) in atherosclerosis. NcRNAs are involved in epigenetic regulation of endothelial function, SMC proliferation, cholesterol synthesis, lipid metabolism, and inflammatory response.

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Section: Atherosclerosis and Epigenetic Modificationsmentioning

confidence: 99%

Epigenetic Reprogramming in Atherosclerosis

Grimaldi

Vietri

Schiano

et al. 2014

Curr Atheroscler Rep

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“…Furthermore, previous studies have found that individuals with DNA repair deficiencies show an increased sensitivity to CAD [16–18]. In addition, several epidemiological studies have revealed that these two variations in the XRCC1 gene influence DNA repair and are associated with an increased susceptibility to CAD [19–21].…”

Section: Introductionmentioning

confidence: 99%

Associations between XRCC1 Gene Polymorphisms and Coronary Artery Disease: A Meta-Analysis

Ma¹,

Han²,

Wang³

et al. 2016

PLoS ONE

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Genetic variations that influence DNA repair efficiency may contribute to coronary artery disease (CAD) susceptibility. Previous studies have investigated whether there was evidence of an association between polymorphisms at the X-ray repair cross complementing 1 (XRCC1) gene and susceptibility to CAD, but findings have been inconclusive. We identified eligible studies through a comprehensive literature search to determine whether an association exists between XRCC1 gene polymorphisms and CAD susceptibility. Findings were assessed using the odds ratio (OR) and corresponding 95% confidence interval (CI), which were calculated using a fixed- or random-effects model, based on the heterogeneity of the studies. Ten eligible studies were finally included in this meta-analysis. Our pooled analysis found that XRCC1 polymorphisms were significantly associated with CAD susceptibility under recessive (Arg194Trp: OR = 1.47, 95% CI = 1.13–1.93; Arg399Gln: OR = 1.45, 95% CI = 1.12–1.89), homozygous (Arg194Trp: OR = 1.37, 95% CI = 1.03–1.81; Arg399Gln: OR = 1.56, 95% CI = 1.19–2.05), and allele (Arg399Gln: OR = 1.18, 95% CI = 1.06–1.32) genetic models. Following subgroup analysis by ethnicity, in Asian populations, we found evidence of associations between the XRCC1 Arg194Trp polymorphism and CAD under recessive and homozygous genetic models, and between the XRCC1 Arg399Gln polymorphism and CAD under recessive, homozygous, and allele genetic models. Subgroup analysis stratified by control source revealed associations between the Arg194Trp and Arg399Gln polymorphisms and susceptibility to CAD under recessive and homozygous modes of inheritance, respectively. In addition, subgroup analysis stratified by sample size found that findings of the Arg194Trp polymorphism in large sample sizes were comparable to those found using pooled eligible studies. Based on our meta-analysis, we concluded that the XRCC1 gene polymorphisms, Arg194Trp and Arg399Gln, are associated with CAD susceptibility, specifically in Asian populations. However, additional, comprehensive and well-designed studies are warranted to confirm these findings.

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“…In-stent neoatherosclerosis (NA), which closely resembles other forms of atherosclerosis, but may be more aggressive, has been identified as a new mechanism of late phase ISR showing almost exclusive involvement with DES [8]. Mechanisms of atherosclerosis and myocardial infarction are programmed by certain genetic mutations [9,10]. Such mutations link myocardial infarction with atherosclerosis and neointimal hyperplasia, and are ultimately responsible for the inter-relationship between a family history of myocardial infarction and DES in-stent restenosis.…”

mentioning

confidence: 97%

Family history of myocardial infarction as a strong independent predictor of in-stent restenosis in the era of drug eluting stents

Liu¹,

Xu²,

Fu³

et al. 2015

International Journal of Cardiology

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DNA modifications in atherosclerosis: From the past to the future

Cited by 48 publications

References 78 publications

Epigenetic Reprogramming in Atherosclerosis

Epigenetic Reprogramming in Atherosclerosis

Associations between XRCC1 Gene Polymorphisms and Coronary Artery Disease: A Meta-Analysis

Family history of myocardial infarction as a strong independent predictor of in-stent restenosis in the era of drug eluting stents

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