A systematic review of microRNAs in patients with hypertrophic cardiomyopathy

Scolari, Fernando Luís; Faganello, Lucas Simonetto; Garbin, Henrique Iahnke; Mattos, Beatriz Piva e; Biolo, Andréia

doi:10.1016/j.ijcard.2020.11.004

Cited by 33 publications

(22 citation statements)

References 49 publications

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“…Furthermore, miRNAs have been studied as biomarkers for myocardial injury and heart failure, for a review [ 13 ]. Even though miRNAs as biomarkers for HCM have been studied, often prespecified sets have been evaluated [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

A Novel miRNA Screen Identifies miRNA-4454 as a Candidate Biomarker for Ventricular Fibrosis in Patients with Hypertrophic Cardiomyopathy

Thottakara

Lund²,

Krämer

et al. 2021

Biomolecules

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(1) Background: Left ventricular hypertrophy, myocardial disarray and interstitial fibrosis are the hallmarks of hypertrophic cardiomyopathy (HCM). Access to the myocardium for diagnostic purposes is limited. Circulating biomolecules reflecting the myocardial disease processes could improve the early detection of HCM. Circulating miRNAs have been found to reflect disease processes in several cardiovascular diseases. (2) Methods: We quantified circulating miRNA molecules in the plasma of 24 HCM and 11 healthy controls using the Human v3 miRNA Expression Assay Kit Code set (Nanostring Tech., Seattle, WA, USA) and validated differentially expressed miRNAs using RT-PCR. (3) Results: In comparison to healthy controls, the levels of six miRNAs (miR-1, miR-3144, miR-4454, miR-495-3p, miR-499a-5p and miR-627-3p) were higher in the plasma of HCM patients than healthy individuals (p < 0.05). Of these, higher levels of miR-1, miR-495 and miR-4454 could be validated by real-time PCR. In addition, elevated miR-4454 levels were significantly correlated with cardiac fibrosis, detected by magnetic resonance imaging in HCM patients. (4) Conclusions: Circulating miR-1, miR-495-3p and miR-4454 levels are elevated in the plasma of HCM patients. To the best of our knowledge, this is the first report showing a correlation between miR-4454 levels and cardiac fibrosis in HCM. This suggests miR-4454 as a potential biomarker for fibrosis in these patients.

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Section: Introductionmentioning

confidence: 99%

A Novel miRNA Screen Identifies miRNA-4454 as a Candidate Biomarker for Ventricular Fibrosis in Patients with Hypertrophic Cardiomyopathy

Thottakara

Lund²,

Krämer

et al. 2021

Biomolecules

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“…Several of the miRNAs, including mir-1-3p, mir-19b, mir-21, mir-29a, mir-155, and mir-221, were related to either hypertrophy or fibrosis. Mir-29a showed a more consistent phenotypic correlation with HCM and could be a potential biomarker [79] (Table 3). Long noncoding RNAs are now emerging as key epigenetic regulators of a myriad of pathophysiologies; in the same study mentioned above by Gao et al, lncRNA expression profiles of HCM patients were revealed.…”

Section: Noncoding Rnas In Hcmmentioning

confidence: 99%

The Emerging Role of Epigenetics in Therapeutic Targeting of Cardiomyopathies

Pagiatakis

Mauro

2021

IJMS

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Cardiomyopathies (CMPs) are a heterogeneous group of myocardial diseases accountable for the majority of cases of heart failure (HF) and/or sudden cardiac death (SCD) worldwide. With the recent advances in genomics, the original classification of CMPs on the basis of morphological and functional criteria (dilated (DCM), hypertrophic (HCM), restrictive (RCM), and arrhythmogenic ventricular cardiomyopathy (AVC)) was further refined into genetic (inherited or familial) and acquired (non-inherited or secondary) forms. Despite substantial progress in the identification of novel CMP-associated genetic variations, as well as improved clinical recognition diagnoses, the functional consequences of these mutations and the exact details of the signaling pathways leading to hypertrophy, dilation, and/or contractile impairment remain elusive. To date, global research has mainly focused on the genetic factors underlying CMP pathogenesis. However, growing evidence shows that alterations in molecular mediators associated with the diagnosis of CMPs are not always correlated with genetic mutations, suggesting that additional mechanisms, such as epigenetics, may play a role in the onset or progression of CMPs. This review summarizes published findings of inherited CMPs with a specific focus on the potential role of epigenetic mechanisms in regulating these cardiac disorders.

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“…Por fim, a avaliação do desarranjo celular com tensor de difusão por ressonância magnética cardíaca, genotipagem, perfil de microRNAs e outros biomarcadores promissores, bem como a avaliação não invasiva de isquemia miocárdica, poderão assegurar uma avaliação mais rigorosa do substrato anatômico e elétrico da doença. 2,6 Porém, sua assimilação à prática clínica diária deve levar em consideração os recursos disponíveis localmente e representará um grande desafio. A busca por novos paradigmas na CMH está em curso e uma avaliação eletrofisiológica mais precisa dos mecanismos da MSC é necessária, podendo complementar ou mesmo suplantar a estratificação de risco de atual.…”

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