Epigenetic Regulation of Heart Failure: Cell Type Matters

Padula, Stephanie L.; Yutzey, Katherine E.

doi:10.1161/circresaha.121.319642

Cited by 3 publications

(2 citation statements)

References 15 publications

(22 reference statements)

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“…Indeed, epigenetic influences, being crucial post-transcriptional triggers, are considered to be powerful regulators of biomechanical and oxidative stresses, systemic and microvascular inflammation, myocardial fibrosis, and endothelial dysfunction (4). Moreover, key epigenetic mechanisms are regarded as promising molecular targets for new therapeutic interventions in HF including cardiac reprogramming, inducible progenitor cell transplantation, stimulation of resident cardiomyocytes differentiation and proliferation, and inhibition of cardiomyocyte apoptosis (5). These approaches are expected to be effective tools to manage HF at the different stages of its natural evolution.…”

Section: Epigenetics In Heart Failure Developing: the Orchestra Of Et...mentioning

confidence: 99%

Editorial: Epigenetics in Heart Failure Developing: The Orchestra of Etiology and Comorbidities

Berezin

Mozoş

Petrovič

2022

Front. Cardiovasc. Med.

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Section: Epigenetics In Heart Failure Developing: the Orchestra Of Et...mentioning

confidence: 99%

Editorial: Epigenetics in Heart Failure Developing: The Orchestra of Etiology and Comorbidities

Berezin

Mozoş

Petrovič

2022

Front. Cardiovasc. Med.

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“…Therefore, there is a great interest in the study of ICM to obtain a better understanding of the pathophysiology underlying the disease. One of the main research foci is epigenomics, which has allowed the identification of epigenetic alterations in ICM patients [2][3][4]. These epigenetic changes are associated with differential expression at the mRNA level of genes described in the development of ICM [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

DNMT3B System Dysregulation Contributes to the Hypomethylated State in Ischaemic Human Hearts

et al. 2022

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A controversial understanding of the state of the DNA methylation machinery exists in ischaemic cardiomyopathy (ICM). Moreover, its relationship to other epigenetic alterations is incomplete. Therefore, we carried out an in-depth study of the DNA methylation process in human cardiac tissue. We showed a dysregulation of the DNA methylation machinery accordingly with the genome-wide hypomethylation that we observed: specifically, an overexpression of main genes involved in the elimination of methyl groups (TET1, SMUG1), and underexpression of molecules implicated in the maintenance of methylation (MBD2, UHRF1). By contrast, we found DNMT3B upregulation, a key molecule in the addition of methyl residues in DNA, and an underexpression of miR-133a-3p, an inhibitor of DNMT3B transcription. However, we found many relevant alterations that would counteract the upregulation observed, such as the overexpression of TRAF6, responsible for Dnmt3b degradation. Furthermore, we showed that molecules regulating Dnmts activity were altered; specifically, SAM/SAH ratio reduction. All these results are in concordance with the Dnmts normal function that we show. Our analysis revealed genome-wide hypomethylation along with dysregulation in the mechanisms of addition, elimination and maintenance of methyl groups in the DNA of ICM. We describe relevant alterations in the DNMT3B system, which promote a normal Dnmt3b function despite its upregulation.

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Discovery of 1,2,4-Triazole-3-thione Derivatives as Potent and Selective DCN1 Inhibitors for Pathological Cardiac Fibrosis and Remodeling

He,

Gao,

Qiao

et al. 2024

J. Med. Chem.

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Epigenetic Regulation of Heart Failure: Cell Type Matters

Cited by 3 publications

References 15 publications

Editorial: Epigenetics in Heart Failure Developing: The Orchestra of Etiology and Comorbidities

Editorial: Epigenetics in Heart Failure Developing: The Orchestra of Etiology and Comorbidities

DNMT3B System Dysregulation Contributes to the Hypomethylated State in Ischaemic Human Hearts

Discovery of 1,2,4-Triazole-3-thione Derivatives as Potent and Selective DCN1 Inhibitors for Pathological Cardiac Fibrosis and Remodeling

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