Evidence map›Paper›PMID 32943906›Full record

ArticlePharmacogenomics and personalized medicine2020

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

Elham Shirazi-Tehrani, Negar Firouzabadi, Gholamhossein Tamaddon, Ehsan Bahramali, Asma Vafadar

Open access · goldAbstract read
In one paragraph

Article in Pharmacogenomics and personalized medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. MicroRNA-1: Diverse role of a small player in multiple cancers.Seminars in cell & developmental biology · 2022
    Review
  8. Article
  9. Identification of the Potential Molecular Mechanism ofComputational and mathematical methods in medicine · 2022
    Article
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Elham Shirazi-TehraniDepartment of Pharmacology & Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.
Negar FirouzabadiDepartment of Pharmacology & Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID 0000-0002-9293-9845
Gholamhossein TamaddonDepartment of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID 0000-0001-8158-6004
Ehsan BahramaliDigestive Disease Research Center, Digestive Disease Research Institute, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Asma VafadarDepartment of Medical Biotechnology, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.ORCID 0000-0002-4255-3880
Shiraz University of Medical Sciences · IRShariati Hospital · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionMicroRNAs (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.

methodsThe 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.

resultsWe demonstrated that miR-1 and miR-214 were significantly upregulated in the treated group compared to the untreated group (

conclusionIn 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.

Indexed as

cardiac hypertrophycarvedilolmicroRNAsystolic heart failureβ-blocker

Identifiers

PMID32943906
PMCPMC7481348
OpenAlexW3081809144

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.