MicroRNAs, heart failure, and aging: potential interactions with skeletal muscle

Murach, Kevin A.; McCarthy, John J.

doi:10.1007/s10741-016-9572-5

Cited by 28 publications

(22 citation statements)

References 128 publications

(159 reference statements)

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“…In the in vivo experiments, inhibition of miRNA-199b caused normalization of the expression of Dyrk1a, a reduction of nuclear NFAT activity, and inhibition of hypertrophy and fibrosis in mouse models of heart failure [101,159]. Changed expressions of miRNA-1, -214, -29b, -342, -7, -107, -126, -125, -122, -423-5p, -320a, -650, -1228, -662, -583, -3175, -21, -22, and -92b have been shown in other studies of heart failure [106,152,156,[160][161][162][163].…”

Section: Heart Failurementioning

confidence: 78%

“…A brief review of selected miRNAs included in the cardiovascular diseases caused by oxidative stress is provided in Table 1. miRNA-199a Downregulated SIRT1 [139] Heart failure miRNA-199b Upregulated calcineurin/NFAT [101,[157][158][159] miRNA-21 Upregulated natriuretic peptide B [156,163] Mef2a-Myocyte-specific enhancer factor 2A, Gata4-Transcription factor GATA-4, GDP-GTP exchange protein-guanosine diphosphate-guanosine triphosphate exchange protein, Cdc42-Cell division control protein 42, Myh7-beta myosin heavy chain, Keap1/Nrf2-Kelch-like ECH-associated protein 1/Nuclear factor erythroid 2-related factor 2, FoxO1-Forkhead box protein O1, Mcl-1-Myeloid cell leukemia 1, MnSOD-manganese-dependent superoxide dismutase, NF-κB-nuclear factor kappa B, TNF-α-tumor necrosis factor alpha, S1P1-Sphingosine-1-phosphate receptor 1, MKK4-Mitogen-activated protein kinase kinase 4, eNOS-Endothelial nitric oxide synthase, INF receptor-interferon receptor, Ogt-O-linked β-N-acetylglucosamine transferase, HO-1-Heme oxygenase 1, SIRT1-sirtuin 1, NFAT-Nuclear factor of activated T cells.…”

Section: Heart Failurementioning

confidence: 99%

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Oxidative Stress-Responsive MicroRNAs in Heart Injury

Kura

Bačová

Kaločayová

et al. 2020

IJMS

137

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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: Heart Failurementioning

confidence: 78%

Section: Heart Failurementioning

confidence: 99%

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Kura

Bačová

Kaločayová

et al. 2020

IJMS

137

View full text Add to dashboard Cite

show abstract

“…Several studies indicate a fundamental role of both muscle specific (myomiRs) and non-muscle specific miRNAs in skeletal muscle differentiation and function89. Interestingly, miRNA dysregulation has been found in many skeletal muscle dystrophies10111213, including DM1 and DM214151617.…”

mentioning

confidence: 99%

Validation of plasma microRNAs as biomarkers for myotonic dystrophy type 1

Perfetti

Greco

Cardani

et al. 2016

Sci Rep

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Non-invasive and simple to measure biomarkers are still an unmet need for myotonic dystrophy type 1 (DM1). Indeed, muscle biopsies can be extremely informative, but their invasive nature limits their application. Extracellular microRNAs are emerging humoral biomarkers and preliminary studies identified a group of miRNAs that are deregulated in the plasma or serum of small groups of DM1 patients. Here we adopted very stringent selection and normalization criteria to validate or disprove these miRNAs in 103 DM1 patients and 111 matched controls. We confirmed that 8 miRNAs out of 12 were significantly deregulated in DM1 patients: miR-1, miR-27b, miR-133a, miR-133b, miR-206, miR-140-3p, miR-454 and miR-574. The levels of these miRNAs, alone or in combination, discriminated DM1 from controls significantly, and correlated with both skeletal muscle strength and creatine kinase values. Interestingly, miR-133b levels were significantly higher in DM1 female patients. Finally, the identified miRNAs were also deregulated in the plasma of a small group (n = 30) of DM2 patients. In conclusion, this study proposes that miRNAs might be useful as DM1 humoral biomarkers.

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“…Age‐related microRNA and TLR signaling dysregulation may contribute to other diseases of aging, such as muscular and cardiovascular diseases . Notably, sarcopenia in older individuals could be associated with microRNA dysregulation, and changes in microRNA signatures in muscle tissues have been observed with aging …”

Section: Diverse Rnas In Evsmentioning

confidence: 99%

RNA in extracellular vesicles

et al. 2017

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Cells release a range of membrane-enclosed extracellular vesicles (EVs) into the environment. Among them, exosomes and microvesicles (collectively measuring 30-1000 nm in diameter) carry proteins, signaling lipids, and nucleic acids from donor cells to recipient cells, and thus have been proposed to serve as intercellular mediators of communication. EVs transport cellular materials in many physiologic processes, including differentiation, stem cell homeostasis, immune responses, and neuronal signaling. EVs are also increasingly recognized as having a direct role in pathological processes, notably cancer and neurodegeneration. Accordingly, EVs have been the focus of intense investigation as biomarkers of disease and prognostic indicators, and even therapeutic tools. Here, we review the classes of RNAs present in EVs, both coding RNAs (mRNAs) and noncoding RNAs (long noncoding RNAs, microRNAs, and circular RNAs). The rising attention to EV-resident RNAs as biomarkers stems from the fact that RNAs can be detected at extremely low quantities using a number of methods. To illustrate the interest in EV biology, we discuss EV RNAs in cancer and neurodegeneration, two major age-associated disease processes.

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MicroRNAs, heart failure, and aging: potential interactions with skeletal muscle

Cited by 28 publications

References 128 publications

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Oxidative Stress-Responsive MicroRNAs in Heart Injury

Validation of plasma microRNAs as biomarkers for myotonic dystrophy type 1

RNA in extracellular vesicles

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