MicroRNA-133a improves the cardiac function and fibrosis through inhibiting Akt in heart failure rats

Sang, Haiqiang; Jiang, Zhengming; Zhao, Qiuping; Fu, Xin

doi:10.1016/j.biopha.2015.02.030

Cited by 48 publications

(39 citation statements)

References 14 publications

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“…In another murine TAC‐induced hypertrophy model, inhibition of miR‐133 by an antimir resulted in myocardial hypertrophy and left ventricular dilatation, whereas overexpression induced by an adenovirus containing a miR‐133 mimic led to a decrease in hypertrophy by means of Akt activation . A recent study confirmed the regulatory role of miR‐133a in the Akt pathway and showed a beneficial effect of a miR‐133a mimic on cardiac function in heart failure rats …”

Section: Therapeutic Microrna‐based Strategies In Heart Failurementioning

confidence: 92%

“…74 A recent study confirmed the regulatory role of miR-133a in the Akt pathway and showed a beneficial effect of a miR-133a mimic on cardiac function in heart failure rats. 87 In 2011, Ucar et al 88 reported on the miR-212/132 family which are known to regulate cardiac hypertrophy by targeting the FoxO3 transcription factor. Overexpression of miR-212 and miR-132 in mice led to a phenotype with an increase in cardiac hypertrophy and heart failure; however, after administration of a miR-132 antimir, cardiac hypertrophy and heart failure development were attenuated.…”

Section: Figurementioning

confidence: 99%

See 1 more Smart Citation

MicroRNAs in heart failure: from biomarker to target for therapy

Vegter

Meer

Windt

et al. 2016

European J of Heart Fail

252

192

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MicroRNAs (miRNAs) are increasingly recognized to play important roles in cardiovascular diseases, including heart failure. These small, non-coding RNAs have been identified in tissue and are involved in several pathophysiological processes related to heart failure, such as cardiac fibrosis and hypertrophy. As a result, miRNAs have become interesting novel drug targets, leading to the development of miRNA mimics and antimirs. MicroRNAs are also detected in the circulation, and are proposed as potential diagnostic and prognostic biomarkers in heart failure. However, their role and function in the circulation remains to be resolved. Here, we review the potential roles of miRNAs as circulating biomarkers and as targets for therapy.

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Section: Therapeutic Microrna‐based Strategies In Heart Failurementioning

confidence: 92%

Section: Figurementioning

confidence: 99%

MicroRNAs in heart failure: from biomarker to target for therapy

Vegter

Meer

Windt

et al. 2016

European J of Heart Fail

252

192

View full text Add to dashboard Cite

show abstract

“…It has been observed that the levels of miR‐133a are significantly reduced in fibrotic hearts, and its overexpression abrogates cardiac fibrosis in a coronary artery ligation‐induced rat model of heart failure and improves cardiac structure and function. This study further unveiled the molecular basis as it showed that miR‐133a activates AKT phosphorylation and AKT inhibitor triciribine hydrate (TCN) blocks the cardioprotective effect of miR‐133a (Sang et al, ). A recent study demonstrated that the levels of endomyocardial miR‐133a are significantly higher in inflammatory cardiomyopathy (iCAMP) patients with preserved LV function and less myocardial fibrosis than iCAMP patients with reduced LV function (Besler et al, ) further indicating the anti‐fibrotic and cardioprotective role of miR‐133a and a potential target for fibrosis therapy.…”

Section: Contributions Of Epigenetic Regulators In Fibrogenesismentioning

confidence: 88%

Epigenetics in Reactive and Reparative Cardiac Fibrogenesis: The Promise of Epigenetic Therapy

Ghosh

Rai

Flevaris

et al. 2017

Journal Cellular Physiology

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Epigenetic changes play a pivotal role in the development of a wide spectrum of human diseases including cardiovascular diseases, cancer, diabetes, and intellectual disabilities. Cardiac fibrogenesis is a common pathophysiological process seen during chronic and stress-induced accelerated cardiac aging. While adequate production of extracellular matrix (ECM) proteins is necessary for post-injury wound healing, excessive synthesis and accumulation of extracellular matrix protein in the stressed or injured hearts causes decreased or loss of lusitropy that leads to cardiac failure. This self-perpetuating deposition of collagen and other matrix proteins eventually alter cellular homeostasis; impair tissue elasticity and leads to multi-organ failure, as seen during pathogenesis of cardiovascular diseases, chronic kidney diseases, cirrhosis, idiopathic pulmonary fibrosis, and scleroderma. In the last 25 years, multiple studies have investigated the molecular basis of organ fibrosis and highlighted its multi-factorial genetic, epigenetic, and environmental regulation. In this minireview, we focus on five major epigenetic regulators and discuss their central role in cardiac fibrogenesis. Additionally, we compare and contrast the epigenetic regulation of hypertension-induced reactive fibrogenesis and myocardial infarction-induced reparative or replacement cardiac fibrogenesis. As microRNAs-one of the major epigenetic regulators-circulate in plasma, we also advocate their potential diagnostic role in cardiac fibrosis. Lastly, we discuss the evolution of novel epigenetic-regulating drugs and predict their clinical role in the suppression of pathological cardiac remodeling, cardiac aging, and heart failure. J. Cell. Physiol. 232: 1941-1956, 2017. © 2016 Wiley Periodicals, Inc.

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“…Reportedly, mice lacking miR-1-2 develop ventricular septal abnormalities and cardiac rhythm disturbances [43]. While the deficiency of miR-133a leads to myocardial matrix remodeling and progress of heart failure [44, 45]. Further pathway analysis indicated that gap junction pathway was the predicted closely correlation pathway to be targeted by miR-1 and miR-133.…”

Section: Discussionmentioning

confidence: 99%

miRNA Expression Profile and Effect of Wenxin Granule in Rats with Ligation-Induced Myocardial Infarction

Lou

Zhai³

et al. 2017

International Journal of Genomics

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Wenxin Granule (WXKL) is a traditional Chinese medicine used for treatment of myocardial infarction (MI) and arrhythmias. However, the genomic pathological mechanisms of MI and mechanisms of WXKL are largely unknown. This study aims to investigate a comprehensive miRNA expression profile, and the predicted correlation pathways to be targeted by differentially expressed miRNAs in MI, and mechanisms of WXKL from a gene level. MI rat model was established by a coronary artery ligation surgery. miRNA expression microarrays were performed and the data were deposited in Gene Expression Omnibus (GEO number GSE95855). And, pathway analysis was performed by using the DIANA-miRPath v3.0 online tool. The expressions of miR-1, miR-133, Cx43, and Cx45 were detected by quantitative real-time PCR. It was found that 35 differentially expressed miRNAs and 23 predicted pathways, including miR-1, miR-133, and gap junction pathway, are involved in the pathogenesis of MI. And, WXKL increased the expressions of miR-1 and miR-133, while also increased the mRNA levels of Cx43 and Cx45, and, especially, recovered the Cx43/Cx45 ratio near to normal level. The results suggest that regulatory effects on miR-1, miR-133, Cx43, and Cx45 might be a possible mechanism of WXKL in the treatment of MI at the gene level.

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MicroRNA-133a improves the cardiac function and fibrosis through inhibiting Akt in heart failure rats

Cited by 48 publications

References 14 publications

MicroRNAs in heart failure: from biomarker to target for therapy

MicroRNAs in heart failure: from biomarker to target for therapy

Epigenetics in Reactive and Reparative Cardiac Fibrogenesis: The Promise of Epigenetic Therapy

miRNA Expression Profile and Effect of Wenxin Granule in Rats with Ligation-Induced Myocardial Infarction

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