MicroRNA-133a regulates DNA methylation in diabetic cardiomyocytes

Chavali, Vishalakshi; Tyagi, Suresh C.; Mishra, Paras Kumar

doi:10.1016/j.bbrc.2012.07.105

Cited by 59 publications

(46 citation statements)

References 33 publications

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“…In agreement, a recent report shows miR-133a to be attenuated and contribute to cardiac hypertrophy in diabetic hearts [49] while overexpression of miR-133a attenuates cardiac fibrosis in diabetics [50]. These effects are related to control of DNA methylation by miR-133 via direct regulation of DNA methyl transferases in diabetic cardiomyocytes [51]. The role of miR-133 in regulating cardiac hypertrophy, fibrosis, epigenetic modification, and β-AR signaling points miR-133 as a promising therapeutic target in managing HF.…”

Section: Angiogenesissupporting

confidence: 71%

Targeting microRNAs in heart failure

Duygu

Windt

Martins

2016

Trends in Cardiovascular Medicine

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Section: Angiogenesissupporting

confidence: 71%

Targeting microRNAs in heart failure

Duygu

Windt

Martins

2016

Trends in Cardiovascular Medicine

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“…Furthermore, analysis of miR expression levels in the hearts of various rat and mouse diabetic models also indicated the abnormal expression of miRNA. Further studies demonstrated that miRs contribute to numerous important pathophysiological processes of DCM, including cardiomyocyte hypertrophy, myocardial fibrosis, cardiomyocyte apoptosis, mitochondrial dysfunction, myocardial electrical remodeling and epigenetic modification (27)(28)(29)(30)(31)(32). The present review discusses the possible role of miRs in the pathogenesis of DCM regarding the above-mentioned processes.…”

Section: Introductionmentioning

confidence: 88%

“…In addition to its role in mediating myocardial hypertrophy and fibrosis, miR-133a was found to contribute to hyperglycemia-mediated DNA hypermethylation by regulating the expression levels of DNA methyl transferases, which catalyze DNA methylation. It was observed that the expression of miR-133a was attenuated while DNA methyl transferase (Dnmt)-1 and -3b were induced in Ins2 +/-Akita hearts, and overexpression of miR-133a inhibits, but silencing of miR-133a induces, Dnmt-1, -3a and -3b, demonstrating the involvement of miR-133a in the regulation of DNA methylation (27).…”

Section: Mirs In Cardiomyocyte Apoptosis and Mitochondrial Dysfunctionmentioning

confidence: 99%

“…miRs are also involved in the pathogenesis of DCM through participating in various pathophysiological processes, such as myocardial electrical remodeling and epigenetic modification (27,31). A significant increase in the level of miR-301 expression and reduction of the voltage gated potassium channel, Kv4.2 expression level were observed in the diabetic (db/db mice) ventricles and miR-301 was validated to modulate Kv4.2 by direct binding on its 3'-UTR (31).…”

Section: Mirs In Cardiomyocyte Apoptosis and Mitochondrial Dysfunctionmentioning

confidence: 99%

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Role of microRNAs in the pathogenesis of diabetic cardiomyopathy

Liu

2017

Biomedical Reports

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Abstract. The morbidity of diabetes mellitus has been increasing annually. As a progressive metabolic disorder, chronic complications occur in the late stage of diabetes. In addition, cardiovascular diseases account for the major cause of morbidity and mortality among the diabetic population worldwide. Diabetic cardiomyopathy (DCM) is a type of diabetic heart disease. Patients with DCM show symptoms and signs of heart failure while no specific cause, such as coronary disease, hypertension, alcohol consumption, or other structural heart diseases has been identified. The pathogenesis of DCM is complex and has not been well understood until recently. MicroRNAs (miRs) belong to a novel family of highly conserved, short, non-coding, single-stranded RNA molecules that regulate transcriptional and post-transcriptional gene expression. Furthermore, recent studies have demonstrated an association between miRs and DCM. In the current review, the role of miRs in the pathogenesis of DCM is summarized. It was concluded that miRs contribute to the regulation of cardiomyocyte hypertrophy, myocardial fibrosis, cardiomyocyte apoptosis, mitochondrial dysfunction, myocardial electrical remodeling, epigenetic modification and various other pathophysiological processes of DCM. These studies may provide novel insights into targets for prevention and treatment of the disease.

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“…On the other hand, higher miRNA-133 expression has been associated with low-grade heart failure (36) and antiapoptotic effects (37). The role of alterations of miRNA-133 has been demonstrated in remodeling processes leading to cardiomyocyte hypertrophy in diabetes (38,39). Interestingly, miRNA-133 is likely essential for regeneration of the injured heart (40).…”

Section: Tab 2 Correlation Of Mirnas Expression To Selected Clinicamentioning

confidence: 99%

MicroRNAs in pathophysiology of acute myocardial infarction and cardiogenic shock

Mp¹,

Lipková²,

J³

et al. 2018

BLL

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AIM: Levels of circulating miRNA are considered to be potential biomarkers of acute myocardial infarction and disease progression. METHODS: In this study, the expression levels of circulating miRNA-1, miRNA-133 and miRNA-124a were investigated in a group of patients with acute myocardial infarction (STEMI) and cardiogenic shock (CS) compared to controls. RESULTS: During the hospitalization period, miRNA-133 showed a signifi cant up-regulation in the serum of STEMI and CS patients compared to controls, while the expression of miRNA-1 was signifi cantly different only in CS. The expression of miRNA-124 was signifi cantly higher in STEMI and CS. Furthermore, miRNA-1 expression was related to the level of circulating glucose in patients with STEMI. We also found a negative correlation between miRNA-133 and MMP-9 levels. MiRNA-124 expression was signifi cantly related to the level of soluble ST2; the marker correlated to cardiac damage. CONCLUSION: All selected miRNAs are potential markers of cardiac injury in cardiogenic shock, whereas miRNA-124a and -133 are markers of injury in STEMI. MiRNA-1 expression is related to circulating glucose in STEMI. None of miRNAs could be correlated to the extent of injury, progress of the disease, or prognosis of patient outcome. Therefore, the levels of circulating miRNA have no potential for becoming a biomarker of myocardial damage and as such would bring no further benefi t compared to current markers (Tab. 4, Fig. 1, Ref. 47). Text in PDF www.elis.sk.

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MicroRNA-133a regulates DNA methylation in diabetic cardiomyocytes

Cited by 59 publications

References 33 publications

Targeting microRNAs in heart failure

Targeting microRNAs in heart failure

Role of microRNAs in the pathogenesis of diabetic cardiomyopathy

MicroRNAs in pathophysiology of acute myocardial infarction and cardiogenic shock

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