Up-regulation of MSH2, XRCC1 and ATM genes in patients with type 2 diabetes and coronary artery disease

Ahmadi, Amirhossein; Behmanesh, Mehrdad; Boroumand, Mohammad Ali; Tavallaei, Mahmood

doi:10.1016/j.diabres.2015.05.049

Cited by 21 publications

(13 citation statements)

References 34 publications

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“…These reactions include activation of DNA repair, cell cycle checkpoints, and apoptosis by the activation of downstream targets (Khanna, Lavin, Jackson, & Mulhern, 2001; Rotman & Shiloh, 1998). ATM is significantly overexpressed in patients with serious multivessel coronary artery disease compared with single‐vessel disease individuals based on angiography data (Ahmadi et al, 2015). MI upregulates ATM protein expression levels (Daniel et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

“…ATM also coordinates the cellular response to DNA damage and triggers apoptosis through p53 phosphorylation (Banin et al, 1998). A growing body of evidence has demonstrated that ATM expression plays an important role in coronary artery disease (Ahmadi, Behmanesh, Boroumand, & Tavallaei, 2015). ATM −/− mice had a significant reduction in hepatocellular apoptosis and fibrosis compared with ATM +/+ or ATM +/− mice in a high‐fat diet‐fed model (Daugherity et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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miR‐26a attenuates cardiac apoptosis and fibrosis by targeting ataxia–telangiectasia mutated in myocardial infarction

Chiang

Liang

Lin

et al. 2020

Journal Cellular Physiology

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Apoptosis and fibrosis play a vital role in myocardial infarction (MI) induced tissue injury. Although microRNAs have been the focus of many studies on cardiac apoptosis and fibrosis in MI, the detailed effects of miR-26a is needed to further understood. The present study demonstrated that miR-26a was downregulated in ST-elevation MI (STEMI) patients and oxygen-glucose deprivation (OGD)-treated H9c2 cells. Downregulation of miR-26a was closely correlated with the increased expression of creatine kinase, creatine kinase-MB and troponin I in STEMI patients. Further analysis identified that ataxia-telangiectasia mutated (ATM) was a target gene for miR-26a based on a bioinformatics analysis. miR-26a overexpression effectively reduced ATM expression, apoptosis, and apoptosis-related proteins in OGD-treated H9c2 cells. In a mouse model of MI, the expression of miR-26a was significantly decreased in the infarct zone of the heart, whereas apoptosis and ATM expression were increased. miR-26a overexpression effectively reduced ATM expression and cardiac apoptosis at Day 1 after MI. Furthermore, we demonstrated that overexpression of miR-26a improved cardiac function and reduced cardiac fibrosis by the reduced expression of collagen type I and connective tissue growth factor (CTGF) in mice at Day 14 after MI. Overexpression of miR-26a or ATM knockdown decreased collagen I and CTGF expression in cultured OGD-treated cardiomyocytes. Taken together, these data demonstrate a prominent role for miR-26a in linking ATM expression to ischemia-induced apoptosis and fibrosis, key Chiang-Wen Lee and Mao-Shin Lin contributed equally to this work.features of MI progression. miR-26a reduced MI development by affecting ATM expression and could be targeted in the treatment of MI.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR‐26a attenuates cardiac apoptosis and fibrosis by targeting ataxia–telangiectasia mutated in myocardial infarction

Chiang

Liang

Lin

et al. 2020

Journal Cellular Physiology

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“…Ahmadi et al [28] reported increased expression of the XRCC1 gene in patients with CAD when compared with normal people, and Martinet et al [29] found a greater number of DNA strand breaks and an overexpression of the XRCC1 gene in atherosclerotic plaques. Such upregulation may be in response to elevated DNA damage because of atherosclerotic progression.…”

Section: Discussionmentioning

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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“…There is less direct evidence that ATM influences the coronary vasculature. Although ATM is upregulated in patients with coronary artery disease and an absence of ATM delays the onset of inflammation following myocardial infarction, suggesting that ATM may likely mediate microvascular adaptation in these cardiac pathological settings [1,26]. These examples highlight the considerable heterogeneity in microvascular responses to stimuli.…”

Section: Aging and Coronary Vascular Adaptation-neovascularizationmentioning

confidence: 99%

Adaptation of the Coronary Microcirculation in Aging

LeBlanc

Hoying

2016

Microcirculation

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Advancing age will affect every individual and its impact on health deserves significant attention particularly as we address therapeutic possibilities to pathological conditions. The changes that occur in the coronary vasculature as a result of aging-related senescence set the stage upon which CVD and ischemia can escalate. Because of its importance in health, the consequences of aging on vasculature adaptation must be considered as we identify molecular targets and cell therapies for older patients. To understand the complex relationships between the coronary vasculature and the myocardium, it is important to characterize the unique aged cardiac environment in both locales independent of overlying disease. Therefore, the overall theme of this review is to highlight the biology of aging coronary vasculature and how this promotes a decreased plasticity, exacerbating insults such as ischemia. We will identify potential age-related mechanisms that may contribute to this overall loss of adaptation and regeneration and review potential therapeutic strategies to ameliorate this dysfunction.

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Up-regulation of MSH2, XRCC1 and ATM genes in patients with type 2 diabetes and coronary artery disease

Cited by 21 publications

References 34 publications

miR‐26a attenuates cardiac apoptosis and fibrosis by targeting ataxia–telangiectasia mutated in myocardial infarction

miR‐26a attenuates cardiac apoptosis and fibrosis by targeting ataxia–telangiectasia mutated in myocardial infarction

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

Adaptation of the Coronary Microcirculation in Aging

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