MicroRNAs: um novo paradigma no tratamento e diagnóstico da insuficiência cardíaca?

Oliveira-Carvalho, Vagner; Carvalho, Vitor Oliveira; Silva, Miguel Morita; Guimarães, Guilherme Veiga; Bocchi, Edimar Alcides

doi:10.1590/s0066-782x2012000400011

Cited by 31 publications

(15 citation statements)

References 46 publications

(56 reference statements)

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“…The second approach uses antagomirs, chemically designed oligonucleotides. These oligonucleotides specifically inhibit target miRNA by binding to them, which leads to reduction of RISC activation and to upregulation of genes [172,173]. MiRNAs could be modulated also by miRNA sponges (target mimicry), masking, and erasers.…”

Section: Future Perspectives Of Using Mirna In Disease Diagnosis and mentioning

confidence: 99%

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Kura

Bačová

Kaločayová

et al. 2020

IJMS

127

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Reactive oxygen species (ROS) are important molecules in the living organisms as a part of many signaling pathways. However, if overproduced, they also play a significant role in the development of cardiovascular diseases, such as arrhythmia, cardiomyopathy, ischemia/reperfusion injury (e.g., myocardial infarction and heart transplantation), and heart failure. As a result of oxidative stress action, apoptosis, hypertrophy, and fibrosis may occur. MicroRNAs (miRNAs) represent important endogenous nucleotides that regulate many biological processes, including those involved in heart damage caused by oxidative stress. Oxidative stress can alter the expression level of many miRNAs. These changes in miRNA expression occur mainly via modulation of nuclear factor erythroid 2-related factor 2 (Nrf2), sirtuins, calcineurin/nuclear factor of activated T cell (NFAT), or nuclear factor kappa B (NF-κB) pathways. Up until now, several circulating miRNAs have been reported to be potential biomarkers of ROS-related cardiac diseases, including myocardial infarction, hypertrophy, ischemia/reperfusion, and heart failure, such as miRNA-499, miRNA-199, miRNA-21, miRNA-144, miRNA-208a, miRNA-34a, etc. On the other hand, a lot of studies are aimed at using miRNAs for therapeutic purposes. This review points to the need for studying the role of redox-sensitive miRNAs, to identify more effective biomarkers and develop better therapeutic targets for oxidative-stress-related heart diseases.

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Section: Future Perspectives Of Using Mirna In Disease Diagnosis and mentioning

confidence: 99%

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Kura

Bačová

Kaločayová

et al. 2020

IJMS

127

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“…miRNAs are a subset of endogenously-initiated, single-stranded noncoding RNA guide molecules, traceable in organisms as diverse as animals, plants, green algae, and viruses, that regulate gene expression via association with effector complexes (called “micro-ribonucleoprotein” or “miRNP”) and sequence-specific recognition of target sites (also called “cognate mRNAs”), which can dictate the functional outcome [2–5]. They represent one of the most exciting areas of modern medical sciences as they possess unique ability to modulate an immense and complex regulatory network of gene expression [6, 7] in a broad spectrum of developmental and cellular processes including tissue development [8, 9], cell proliferation [10, 11], cell division [12, 13], cell differentiation [14], neuronal asymmetry [15], metabolism [16], stem cell properties [17], apoptosis [18], protein secretion [19], and viral infection [20]. It is becoming clear that they have a big impact on shaping transcriptomes and proteomes of eukaryotes [21].…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of miRNA-Mediated Gene Regulation from Common Downregulation to mRNA-Specific Upregulation

Orang

Safaralizadeh

Kazemzadeh

2014

International Journal of Genomics

451

317

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Discovered in 1993, micoRNAs (miRNAs) are now recognized as one of the major regulatory gene families in eukaryotes. To date, 24521 microRNAs have been discovered and there are certainly more to come. It was primarily acknowledged that miRNAs result in gene expression repression at both the level of mRNA stability by conducting mRNA degradation and the level of translation (at initiation and after initiation) by inhibiting protein translation or degrading the polypeptides through binding complementarily to 3′UTR of the target mRNAs. Nevertheless, some studies revealed that miRNAs have the capability of activating gene expression directly or indirectly in respond to different cell types and conditions and in the presence of distinct cofactors. This reversibility in their posttranslational gene regulatory natures enables the bearing cells to rapidly response to different cell conditions and consequently block unnecessary energy wastage or maintain the cell state. This paper provides an overview of the current understandings of the miRNA characteristics including their genes and biogenesis, as well as their mediated downregulation. We also review up-to-date knowledge of miRNA-mediated gene upregulation through highlighting some notable examples and discuss the emerging concepts of their associations with other posttranscriptional gene regulation processes.

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“…During the last decade, these molecules garnered much attention for their potential as promising new biomarkers for a wide range of diseases with the benefits of both tissue and disease-specific expression signatures and high stability in body fluids [3]. Recently, some circulating miRNAs such as miR-1, -146a, -133b, -208a, -208b and -423-5p have been suggested as earlier biomarkers of myocardial injury, heart failure and/or drug-induced cardiotoxicity [4, 5].…”

Section: Introductionmentioning

confidence: 99%

Circulating miR-1 as a potential biomarker of doxorubicin-induced cardiotoxicity in breast cancer patients

et al. 2016

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Cardiotoxicity is associated with the chronic use of doxorubicin leading to cardiomyopathy and heart failure. Identification of cardiotoxicity-specific miRNA biomarkers could provide clinicians with a valuable prognostic tool. The aim of the study was to evaluate circulating levels of miRNAs in breast cancer patients receiving doxorubicin treatment and to correlate with cardiac function. This is an ancillary study from “Carvedilol Effect on Chemotherapy-induced Cardiotoxicity” (CECCY trial), which included 56 female patients (49.9±3.3 years of age) from the placebo arm. Enrolled patients were treated with doxorubicin followed by taxanes. cTnI, LVEF, and miRNAs were measured periodically. Circulating levels of miR-1, -133b, -146a, and -423-5p increased during the treatment whereas miR-208a and -208b were undetectable. cTnI increased from 6.6±0.3 to 46.7±5.5 pg/mL (p<0.001), while overall LVEF tended to decrease from 65.3±0.5 to 63.8±0.9 (p=0.053) over 12 months. Ten patients (17.9%) developed cardiotoxicity showing a decrease in LVEF from 67.2±1.0 to 58.8±2.7 (p=0.005). miR-1 was associated with changes in LVEF (r=-0.531, p<0.001). In a ROC curve analysis miR-1 showed an AUC greater than cTnI to discriminate between patients who did and did not develop cardiotoxicity (AUC = 0.851 and 0.544, p= 0.0016). Our data suggest that circulating miR-1 might be a potential new biomarker of doxorubicin-induced cardiotoxicity in breast cancer patients.

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MicroRNAs: um novo paradigma no tratamento e diagnóstico da insuficiência cardíaca?

Cited by 31 publications

References 46 publications

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Mechanisms of miRNA-Mediated Gene Regulation from Common Downregulation to mRNA-Specific Upregulation

Circulating miR-1 as a potential biomarker of doxorubicin-induced cardiotoxicity in breast cancer patients

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