<i>miR-139-5p</i> inhibits isoproterenol-induced cardiac hypertrophy by targetting c-Jun

Su, Ming; Wang, Shuiyun; Qiu, Wei; Li, Jianhui; Hui, Rutai; Song, Lingyun; Jia, Mei; Wang, Hui; Wang, Jizheng

doi:10.1042/bsr20171430

Cited by 26 publications

(19 citation statements)

References 35 publications

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“…MiR-139-5p was found to be one of the most downregulated miRNAs in HCM patient hearts [58]. This result was confirmed in a recent study where the expression of miR-139-5p was reduced in left ventricular tissues of HCM patients [59].…”

Section: Mirnas and Inherited Cardiomyopathiesmentioning

confidence: 59%

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: Mirnas and Inherited Cardiomyopathiesmentioning

confidence: 59%

MicroRNAs in Cardiac Diseases

Colpaert

Calore

2019

Cells

150

117

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“…MiR-10a inhibits cardiac hypertrophy by downregulating the expression of T-box5, a transcription factor involved in cardiac development [61]. Both miR-672-5p and miR-139-5p ameliorate cardiac hypertrophy in cardiomyocytes by inhibiting the expression of another transcription factor c-Jun, a subunit of activator protein-1 (AP-1) [68,69]. Similarly, miR-150 mimics were shown to abrogate glucose-induced cardiomyocyte hypertrophy by repressing the expression of p300, a cofactor for various hypertrophy-responsive transcription factors [70].…”

Section: Micrornas That Promote Cardiac Hypertrophymentioning

confidence: 99%

MicroRNAs in Cardiac Hypertrophy

Wehbe

Nasser

Pintus

et al. 2019

IJMS

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Like other organs, the heart undergoes normal adaptive remodeling, such as cardiac hypertrophy, with age. This remodeling, however, is intensified under stress and pathological conditions. Cardiac remodeling could be beneficial for a short period of time, to maintain a normal cardiac output in times of need; however, chronic cardiac hypertrophy may lead to heart failure and death. MicroRNAs (miRNAs) are known to have a role in the regulation of cardiac hypertrophy. This paper reviews recent advances in the field of miRNAs and cardiac hypertrophy, highlighting the latest findings for targeted genes and involved signaling pathways. By targeting pro-hypertrophic genes and signaling pathways, some of these miRNAs alleviate cardiac hypertrophy, while others enhance it. Therefore, miRNAs represent very promising potential pharmacotherapeutic targets for the management and treatment of cardiac hypertrophy.

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“…and miR-411 were down-regulated during heart failure (Tables 1 and 2). Among the seven up-regulated miRs, three miRs (miR-92b, miR-139 and miR-378a) are known to be anti-hypertrophic [31][32][33][34] and another three miRs (miR-139, miR-378a and miR-345) are anti-fibrotic [35][36][37] (Table 5). These data indicate that up-regulated miRs are likely involved in the cardioprotective function.…”

Section: Discussionmentioning

confidence: 99%

Analysis of extracellular vesicle miRNA profiles in heart failure

Lee

Gordon

et al. 2020

J Cellular Molecular Medi

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A heart is a highly complex structure composed of multiple types of cellular and acellular tissues. 1,2 Of cardiac components, cardiomyocyte is a major contributor to cardiac composition and output. 1 Non-myocytes such as fibroblasts, leucocytes and endothelial cells serve as a spatial buffer and more importantly modulate cardiomyocyte functions in response to physiological and pathological stimuli. Thus, cardiomyocytes and non-myocytes closely communicate to maintain cardiac homeostasis, and the imbalance in this communication causes cardiac diseases. 3 Metabolites such as nitric oxide and reactive oxygen species and signalling molecules including extracellular matrix proteins, cytokines and growth factors are known to be classic mediators of intercellular communication. 3,4 Recently, extracellular vesicles (EVs) emerged as a mechanism underlying this intercellular communication. Although EVs had incipiently been considered as a means of cellular waste disposal, accumulating data recently indicated that genetic cargos such as mRNAs,

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miR-139-5p inhibits isoproterenol-induced cardiac hypertrophy by targetting c-Jun

Cited by 26 publications

References 35 publications

MicroRNAs in Cardiac Diseases

MicroRNAs in Cardiac Diseases

MicroRNAs in Cardiac Hypertrophy

Analysis of extracellular vesicle miRNA profiles in heart failure

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