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Carvedilol Alters Circulating MiR-1 and MiR-214 in Heart Failure

Authors Shirazi-Tehrani E, Firouzabadi N, Tamaddon G, Bahramali E, Vafadar A

Received 1 June 2020

Accepted for publication 11 August 2020

Published 3 September 2020 Volume 2020:13 Pages 375—383

DOI https://doi.org/10.2147/PGPM.S263740

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Martin Bluth


Elham Shirazi-Tehrani,1 Negar Firouzabadi,1,2 Gholamhossein Tamaddon,3,4 Ehsan Bahramali,5 Asma Vafadar3,4

1Department of Pharmacology & Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran; 2Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran; 3Department of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran; 4Diagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran; 5Digestive Disease Research Center, Digestive Disease Research Institute, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran

Correspondence: Negar Firouzabadi
Department of Pharmacology & Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran
Tel +98-917-314-5303
Email nfirouzabadi@yahoo.com
Gholamhossein Tamaddon
Department of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran
Tel +98-915-141-7043
Email tamaddon.g@gmail.com

Introduction: MicroRNAs (miRNAs) are recognized as major contributors in various cardiovascular diseases, such as heart failure (HF). These small noncoding RNAs that posttranscriptionally control target genes are involved in regulating different pathophysiological processes including cardiac proliferation, ifferentiation, hypertrophy, and fibrosis. Although carvedilol, a β-adrenergic blocker, and a drug of choice in HF produce cytoprotective actions against cardiomyocyte hypertrophy, the mechanisms are poorly understood. Here we proposed that the expression of hypertrophic-specific miRNAs (miR-1, miR-133, miR-208, and miR-214) might be linked to beneficial effects of carvedilol.
Methods: The levels of four hypertrophic-specific miRNAs were measured in the sera of 35 patients with systolic HF receiving carvedilol (treated) and 20 HF patients not receiving any β-blockers (untreated) as well as 17 nonHF individuals (healthy) using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Systolic HF was defined as left ventricular ejection fraction < 50% by transthoracic echocardiography.
Results: We demonstrated that miR-1 and miR-214 were significantly upregulated in the treated group compared to the untreated group (P=0.014 and 5.3-fold, 0.033 and 4.2-fold, respectively). However, miR-133 and miR-208 did not show significant difference in expression between these two study groups. MiR-1 was significantly downregulated in the untreated group compared with healthy individuals (P=0.019 and 0.14-fold).
Conclusion: In conclusion, it might be postulated that one of the mechanisms by which carvedilol may exert its cardioprotective effects can be through increasing miR-1 and miR-214 expressions which may also serve as a potential therapeutic target in patients with systolic HF in future.

Keywords: microRNA, β-blocker, carvedilol, systolic heart failure, cardiac hypertrophy

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