MicroRNA-copy number variations in coronary artery disease patients with or without type 2 diabetes mellitus

Sohrabifar, Nasim; Ghaderian, Sayyed Mohammad Hossein; Vakili, Hosein; Ghaedi, Hamid; Rouhani, Borzu; Jafari, Hossein; Heidari, Laleh

doi:10.1080/13813455.2019.1651340

Cited by 11 publications

(3 citation statements)

References 44 publications

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“…Finally, several SNPs and CNVs within miRNA coding genes have been associated with risk of CAD, providing further evidence for crucial partake of miRNAs in the pathogenesis of CAD. Most notably, some genotypes of these SNPs have been associated with risk of CAD in patients with specific lifestyles or habits (61,62), demonstrating the possible interaction between these genetic variants and environmental factors. However, the impact of these SNPs on CAD-related biological processes such as cell adhesion, inflammation, proliferation or apoptosis has not been appraised in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…They have reported remarkable differences in the distribution of CNVs of hsa-miR-93 between CAD and non-CAD as well as between diabetic CAD and diabetic non-CAD individuals. In addition, hsa-miR-122 CNVs have been differently distributed among three subgroups (62). The rs2292832 miR-149 has been associated with risk of CAD in Iranian population.…”

Section: Mirna Polymorphisms and Copy Number Variations In Cadmentioning

confidence: 95%

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Role of MicroRNAs in the Pathogenesis of Coronary Artery Disease

Ghafouri‐Fard

Gholipour

Taheri

2021

Front. Cardiovasc. Med.

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Coronary artery disease (CAD) is the main reason of cardiovascular mortalities worldwide. This condition is resulted from atherosclerotic occlusion of coronary arteries. MicroRNAs (miRNAs) are implicated in the regulation of proliferation and apoptosis of endothelial cells, induction of immune responses and different stages of plaque formation. Up-regulation of miR-92a-3p, miR-206, miR-216a, miR-574-5p, miR-23a, miR-499, miR-451, miR-21, miR-146a, and a number of other miRNAs has been reported in CAD patients. In contrast, miR-20, miR-107, miR-330, miR-383-3p, miR-939, miR-4306, miR-181a-5p, miR-218, miR-376a-3p, and miR-3614 are among down-regulated miRNAs in CAD. Differential expression of miRNAs in CAD patients has been exploited to design diagnostic or prognostic panels for evaluation of CAD patients. We appraise the recent knowledge about the role of miRNAs in the development of diverse clinical subtypes of CAD.

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Section: Discussionmentioning

confidence: 99%

Section: Mirna Polymorphisms and Copy Number Variations In Cadmentioning

confidence: 95%

Role of MicroRNAs in the Pathogenesis of Coronary Artery Disease

Ghafouri‐Fard

Gholipour

Taheri

2021

Front. Cardiovasc. Med.

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“…2,3) Stroke diseases such as acute myocardial infarction (AMI) caused by CHD are currently the leading cause of death and disability in the global population. 4) CHD is caused by genetic and environmental factors and their interactions, and a large number of studies have confirmed that diabetes mellitus, hypertension, dyslipidemia, and obesity are routine risk factors for CHD, [5][6][7] but these external factors can only partially explain the cause of CHD. In addition to environmental and genetic factors, there is growing evidence that epigenetic changes may play a key role in the development of CHD.…”

mentioning

confidence: 99%

Expression of lncRNA APF in Peripheral Blood of Patients with Acute Myocardial Infarction Caused by Coronary Heart Disease and its Clinical Significance

Zeng

Duan

et al. 2022

Int. Heart J.

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Coronary heart disease (CHD) is the leading cause of death from cardiovascular disease. This study investigated the expression and clinical significance of long noncoding RNA (lncRNA) autophagy promoting factor (APF) in peripheral blood of patients with acute myocardial infarction (AMI) caused by CHD. Patients with angina pectoris (AP) (n = 80) and AMI (n = 96) and other patients (n = 60) with precordial discomfort but no CHD were included. The serum levels of lncRNA APF, MIAT, MALAT1, H19, CHAST, CDR1AS, miR-188-3 p, and cardiac troponin I (cTnI)/creatine kinase (CK)/creatine kinase isozymes (CK-MB) were detected using reverse transcription-quantitative polymerase chain reaction or enzyme-linked immunosorbent assay. Patients with AMI were divided into high/low expression groups based on the median level of APF, and the clinical baseline indicators of patients with AMI were compared. The correlation between lncRNA APF and cTnI/CK/ CK-MB/miR-188-3p was analyzed using Pearson analysis, and the clinical value of lncRNA APF was evaluated using the receiver operating characteristic curve. The levels of lncRNA APF, MIAT, MALAT1, H19, CHAST, and CDR1AS in patients with AMI were increased, whereas there were no differences in patients with AP. The APF levels in patients with AMI were higher than MIAT, MALAT1, and CHAST, whereas there were no differences between APF and H19 and CDR1AS. In patients with AMI, the high level of lncRNA APF was correlated with the history of smoking/drinking. Moreover, lncRNA APF was positively correlated with cTnI/CK/ CK-MB levels and negatively correlated with miR-188-3p. LncRNA APF has high diagnostic efficacy for AMI. Overall, lncRNA APF is highly expressed in patients with AMI caused by CHD and has high diagnostic efficacy for AMI.

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