The relationship between myocardial fibrosis and myocardial micro<scp>RNA</scp>s in dilated cardiomyopathy: A link between mir‐133a and cardiovascular events

Rubiś, Paweł; Totoń‐Żurańska, Justyna; Wiśniowska‐Śmiałek, Sylwia; Dziewięcka, Ewa; Kołton-Wróż, Maria; Wołkow, Paweł; Pitera, Ewelina; Rudnicka-Sosin, Lucyna; Garlitski, Ann C.; Gackowski, Andrzej; Podolec, Piotr

doi:10.1111/jcmm.13535

Cited by 23 publications

(19 citation statements)

References 16 publications

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“…In a separate study on 55 children affected with DCM, circulating miR-155 and miR-636 were found overexpressed, while miR-646 and miR-639 were downregulated in transplanted patients compared with affected patients who recovered their ventricular function [79]. Also, DCM was associated with altered plasma levels of miR-21, miR-26, miR-29, miR-30, miR-133a [80,81], and with the exosomal miR-92b-5p, found overexpressed in 43 affected patients [82]. Few studies have been performed on ACM, identifying miR-320a and miR-185 significantly down- and upregulated, respectively, in the plasma of affected patients [83,84].…”

Section: Circulating Mirnas As Biomarkers For Cardiac Diseasesmentioning

confidence: 99%

MicroRNAs in Cardiac Diseases

Colpaert

Calore

2019

Cells

150

117

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Since their discovery 20 years ago, microRNAs have been related to posttranscriptional regulation of gene expression in major cardiac physiological and pathological processes. We know now that cardiac muscle phenotypes are tightly regulated by multiple noncoding RNA species to maintain cardiac homeostasis. Upon stress or various pathological conditions, this class of non-coding RNAs has been found to modulate different cardiac pathological conditions, such as contractility, arrhythmia, myocardial infarction, hypertrophy, and inherited cardiomyopathies. This review summarizes and updates microRNAs playing a role in the different processes underlying the pathogenic phenotypes of cardiac muscle and highlights their potential role as disease biomarkers and therapeutic targets.

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Section: Circulating Mirnas As Biomarkers For Cardiac Diseasesmentioning

confidence: 99%

MicroRNAs in Cardiac Diseases

Colpaert

Calore

2019

Cells

150

117

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“…Recent studies have found that miR-133a also regulates cardiomyocyte apoptosis. The expression of miR-133a was decreased in ischemic heart failure, acute myocardial ischemia-reperfusion injury model, and myocardial hypertrophy pathological model in rats [33][34][35][36]. Combined the above research with the results of this experiment, it is suggested that miR-133a-5p may be a key target for the treatment of myocardial injury induced by methamphetamine.…”

Section: Discussionmentioning

confidence: 53%

Expression of miR-133a-5p and ROCK2 in Heart in Methamphetamine-Induced Rats and Intervention of Rhynchophylline

Zhou¹,

Lin²,

Chen³

et al. 2019

Pharmacology

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Introduction: Rhynchophylline, as a traditional Chinese medicine, was used for the treatment of drug addiction. Objective: To investigate miRNAs expression profile in the rat hearts of methamphetamine dependence and the intervention mechanisms of rhynchophylline. Materials and Methods: This study detected the expression profile of miRNAs in the methamphetamine-induced rat hearts by microarray and verified the expression of miR-133a-5P and Rho-associated, coiled-coil containing protein kinase 2 (ROCK2) protein. Results: After conditioned place preference training, methamphetamine significantly increased the time spent in the drug-paired compartment, while rhynchophylline and MK-801 could reduce the time. Cluster analysis results of miRNAs showed that compared with the control group, the expression of miR-133a-5p in methamphetamine-induced rat hearts was decreased significantly; rhynchophylline could significantly increase the expression of miR-133a-5p. The result was verified by real-time polymerase chain reaction. The results of target gene predictive software and related research showed that ROCK2 protein may be the target gene of miR-133a-5p. The immunohistochemistry results of heart tissues showed that the expression of ROCK2 protein was significantly upregulated in the methamphetamine group and downregulate in the rhynchophylline group; the difference between the MK-801 group and the methamphetamine group was not significant. The result of western blot was consistent with the immunohistochemistry. Conclusion: The active ingredient of Chinese herbal medicine rhynchophylline can effectively inhibit the formation of methamphetamine-dependent conditional place preference (CPP) effect in rats to some extent. MiR-133a-5p may participate in the cardioprotective effects of CPP rats by targeting ROCK2.

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“…MiRNAs are reported to be involved in the development of DCM [35][36][37]. Among the dysregulated miRNAs, let-7i has been previously associated with poor clinical outcomes in DCM patients [38].…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown that miRNAs are involved in T-cell immune function and DCM pathogenesis [35][36][37]. Let-7 is reported to not only modulate T-cell function but also regulate glycolytic metabolism.…”

Section: Let-7i Regulated the Metabolic And Functional Alterations Inmentioning

confidence: 99%

Metabolic reprogramming orchestrates CD4+ T-cell immunological status and restores cardiac dysfunction in autoimmune induced-dilated cardiomyopathy mice

Park

Chen

et al. 2019

Journal of Molecular and Cellular Cardiology

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Cellular autoimmune responses, especially those mediated by T-cells, play vital roles in the immunopathogenesis of dilated cardiomyopathy (DCM). Metabolic reprogramming directly controls T-cell function, imprinting distinct functional fates. However, its contribution to T-cell dysfunction and the immunopathogenesis of DCM is unknown. Here, we found that in DCM patients, CD4 + T-cells exhibited immune dysfunction and glycolytic metabolic reprogramming based on extracellular acidification and oxygen consumption rates. Similar results were observed in splenic and cardiac CD4 + T-cells from autoimmune-induced DCM mice. In vitro, the glycolysis inhibitor 2-deoxy-D-glucose (2-DG) reversed T-cell dysfunction; thus, heightened metabolic activity directly controls CD4 + T-cell immunological status. Adoptive transfer of CD4 + T-cells from DCM mice to normal recipients induced cardiac remodeling and cardiac T-cell dysfunction. Strikingly, these effects were abolished by preconditioning cells with 2-DG, indicating that CD4 + T-cell dysfunction partially induced by metabolic reprogramming contributes to cardiac remodeling. Moreover, the microRNA let-7i modulated the metabolism and function of T-cells from DCM mice by directly targeting Myc. Collectively, our results show that metabolic reprogramming occurs in T-cells of autoimmune-induced DCM mice and patients. Further, our findings highlight that glycolytic metabolism is a critical contributor to T-cell dysfunction and DCM immunopathogenesis. Our data position the modulation of the metabolism as a central integrator for T-cell function, representing a promising strategy against autoimmune-mediated DCM progression.

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The relationship between myocardial fibrosis and myocardial microRNAs in dilated cardiomyopathy: A link between mir‐133a and cardiovascular events

Cited by 23 publications

References 16 publications

MicroRNAs in Cardiac Diseases

MicroRNAs in Cardiac Diseases

Expression of miR-133a-5p and ROCK2 in Heart in Methamphetamine-Induced Rats and Intervention of Rhynchophylline

Metabolic reprogramming orchestrates CD4+ T-cell immunological status and restores cardiac dysfunction in autoimmune induced-dilated cardiomyopathy mice

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