scholarly journals Therapeutic Value of miRNAs in Coronary Artery Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Md Sayed Ali Sheikh ◽  
A. Alduraywish ◽  
A. Almaeen ◽  
Mubarak Alruwali ◽  
Raed Alruwaili ◽  
...  

Atherosclerotic ischemic coronary artery disease (CAD) is a significant community health challenge and the principal cause of morbidity and mortality in both developed and developing countries for all ethnic groups. The progressive chronic coronary atherosclerosis is the main underlying cause of CAD. Although enormous progress occurred in the last three decades in the management of cardiovascular diseases, the prevalence of CAD continues to increase worldwide, indicating the need for discovery of deeper molecular insights of CAD mechanisms, biomarkers, and innovative therapeutic targets. Recently, several research groups established that microRNAs essentially regulate various cardiovascular development and functions, and a deregulated cardiac enriched microRNA profile plays a vital role in the pathogenesis of CAD and its biological aging. Numerous studies established that over- or downregulation of a single miRNA gene by ago-miRNA or anti-miRNA is enough to modify the CAD disease process, significantly prevent age-dependent cardiac cell death, and markedly improve cardiac function. In the light of more recent experimental and clinical evidences, we briefly reviewed and discussed the involvement of miRNAs in CAD and their possible diagnostic/therapeutic values. Moreover, we also focused on the role of miRNAs in the initiation and progression of the atherosclerosis plaque as the strongest risk factor for CAD.

MicroRNA ◽  
2020 ◽  
Vol 09 ◽  
Author(s):  
Rashid Mir ◽  
Imadeldin Elfaki ◽  
Chandan k Jha ◽  
Jamsheed Javid ◽  
Suriya Rehman ◽  
...  

Aim: Apart from the modifiable risk factors, genetic factors are believed to also influence the outcome of the coronary artery diseases (CAD). Under the genetic factors, miRNA polymorphisms, namely Hsa-miR-146a-5p (rs2910164) have become an important tool to study the mechanism that underlies the pathogenesis of this disease. Therefore, we investigated the association of miR-146a gene variations with susceptibility of coronary artery diseases. Methodology: This study was conducted on 100 CAD patients and 117 matched healthy individuals. Genotyping of the Hsa-miR-146a-5p C>G gene variation was performed by using amplification refractory mutation system PCR method (ARMS-PCR). Results: The distribution of Hsa-miR-146a-5p rs2910164 C>G genotypes observed between patients and controls was significantly different (P=0.048). Moreover, the frequency of G allele (fG) was found to be significantly higher among patients than in controls (0.36 vs. 0.25). Our findings showed that the Hsa-miR-146a-5p C>G variant was associated with an increased risk of CAD in codominant inheritance model CC vs. CG genotype (OR = 1.84, 95 % CI, 1.02-3.31; p=0.040) and (OR = 3.18, 95 % CI, 1.02-9.9; p=0.045) for CC vs. GG genotype in dominant inheritance model. Whereas the G allele significantly increased the risk of coronary artery disease (OR =1,81, 95 % CI, 1.18-2.78; p=0.006) compared to C allele. Taken together, these results demonstrated that miR-146a/rs2910164 is associated with susceptibility to coronary artery disease, providing novel insights into the genetic etiology and underlying biology of coronary artery disease. Conclusion: Our findings indicated that Hsa-miR-146a-5p rs2910164 GG genotype and G allele are associated with an increased susceptibility to Coronary Artery Disease. A larger sample size can be the key to progress in establishing the genetic co-relation of miRNA gene polymorphisms and cardiovascular diseases.


1981 ◽  
Vol 47 ◽  
pp. 446
Author(s):  
Richard R. Liberthson ◽  
Charles Homcy ◽  
Jay Fallon ◽  
Stephen Gross ◽  
Lawrence Miller

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P5548-P5548
Author(s):  
E. H. A. M. Elsenberg ◽  
J. W. Sels ◽  
S. Van De Weg ◽  
D. P. V. De Kleijn ◽  
N. Pijls ◽  
...  

2019 ◽  
Vol 120 (01) ◽  
pp. 121-131 ◽  
Author(s):  
Jie Gao ◽  
Jia Liu ◽  
Ying Zhang ◽  
BaoYi Guan ◽  
Hua Qu ◽  
...  

AbstractPrethrombotic status (PTS) in patients with stable coronary artery disease (SCAD) increases the risk of coronary thrombosis. Accumulating evidences have indicated that micro-ribonucleic acids (miRNAs) may serve as promising biomarkers for SCAD patients with PTS. The present study aimed to identify the miRNA signature in SCAD patients with PTS and evaluated their diagnostic significance. In the screening phase, 32 differently expressed miRNAs (DEMs) in peripheral blood mononuclear cells (PBMCs) were detected in 35 SCAD patients compared with 5 healthy controls by microarray. MiRNA-gene network analysis was then performed, and 4 DEMs were selected for validation with reverse transcription-quantitative real-time polymerase chain reaction (RT-qPCR) test in an independent cohort comprising 79 SCAD patients and 19 healthy controls. Compared with healthy controls, RT-qPCR test verified the upregulations of miR-34a-5p, miR-432–5p, and miR-370–3p detected by microarray; while the upregulation of miR-495–3p measured by RT-qPCR was not consistent with its low expression detected by microarray. Only miR-34a-5p and miR-495–3p were significantly upregulated in the PTS group compared with the non-PTS group (p < 0.01, p < 0.05). Receiver-operating characteristic (ROC) analysis showed that PBMCs-derived miR-34a-5p and miR-495–3p may discriminate PTS with the areas under the ROC curve (AUC) of 0.780 (confidence interval [CI]95% = 0.673–0.866) and 0.712 (CI95% = 0.599–0.808), respectively. The combination of miR-34a-5p and fibrinogen (FIB, a traditional biomarker for PTS) improved AUC to 0.885 (CI95% = 0.793–0.946) and showed added predictive ability compared with FIB, with an integrated discrimination improvement of 0.201 (p < 0.01). Therefore, the combination of miR-34a-5p and FIB may serve as an efficient tool for distinguishing PTS in SCAD patients.


1995 ◽  
Vol 4 (6) ◽  
pp. 481-484
Author(s):  
BK Valle ◽  
GA Valle ◽  
L Lemberg

Research has lead to a better understanding of the pathophysiology and history of atherosclerotic heart disease, which has reached epidemic proportions in industrialized countries in this century. Atherosclerosis should be seen as a chronic, protracted process that encompasses complex and dynamic interactions between cellular, biochemical, and biophysical factors in the microcosmos of the arterial vessel wall and blood circulation. In this context, the ultimate consequences of this disease process, namely coronary artery disease, must be seen as the "tip of the iceberg." The most dramatic manifestation of coronary artery disease, the acute coronary syndrome, usually occurs as the result of different forces and factors, which lead to abrupt plaque disruption, rupture, and vessel thrombosis. In contrast, the genesis of this atherosclerotic lesion is a slow process. Despite considerable experimental clinical evidence accrued during the past decade, atherosclerosis remains a complex pathophysiological process that is not fully understood. It is clear, however, that the interaction between the cellular elements of the vessel wall and the circulation are the determinants of atheroma formation. In this regard, the vascular endothelium appears to play a pivotal role because of its strategic location and metabolic activity. Antilipidemic therapy influences the outcome of coronary disease through a variety of mechanisms, including direct and indirect effects on the endothelium.


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