Epigenetic regulation and heart failure

Cao, Dian J.

doi:10.1586/14779072.2014.942285

Cited by 7 publications

(2 citation statements)

References 120 publications

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“…On the contrary, Notch and non-canonical Wnt signalling regulate the differentiation events during heart formation [89][90][91][92]. Integrated with the above cardiopoietic growth factors and molecular targets' signaling, non-coding RNAs and epigenetics play a crucial role in cardiac development and myogenic specification of embryonic cardiac progenitors [93][94][95][96]. However, this aspect is beyond the scope of this review and the readers are therefore referred to relevant and elegant reviews on this topics [93][94][95][96][97].…”

Section: Cardiac Morphogens Drive Adult Csc Commitment In Bona-fide Cardiomyocytesmentioning

confidence: 99%

Molecular basis of functional myogenic specification ofBona Fidemultipotent adult cardiac stem cells

et al. 2018

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Ischemic Heart Disease (IHD) remains the developed world's number one killer. The improved survival from Acute Myocardial Infarction (AMI) and the progressive aging of western population brought to an increased incidence of chronic Heart Failure (HF), which assumed epidemic proportions nowadays. Except for heart transplantation, all treatments for HF should be considered palliative because none of the current therapies can reverse myocardial degeneration responsible for HF syndrome. To stop the HF epidemic will ultimately require protocols to reduce the progressive cardiomyocyte (CM) loss and to foster their regeneration. It is now generally accepted that mammalian CMs renew throughout life. However, this endogenous regenerative reservoir is insufficient to repair the extensive damage produced by AMI/IHD while the source and degree of CM turnover remains strongly disputed. Independent groups have convincingly shown that the adult myocardium harbors bona-fide tissue specific cardiac stem cells (CSCs). Unfortunately, recent reports have challenged the identity and the endogenous myogenic capacity of the c-kit expressing CSCs. This has hampered progress and unless this conflict is settled, clinical tests of repair/regenerative protocols are unlikely to provide convincing answers about their clinical potential. Here we review recent data that have eventually clarified the specific phenotypic identity of true multipotent CSCs. These cells when coaxed by embryonic cardiac morphogens undergo a precisely orchestrated myogenic commitment process robustly generating bona-fide functional cardiomyocytes. These data should set the path for the revival of further investigation untangling the regenerative biology of adult CSCs to harness their potential for HF prevention and treatment.

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Section: Cardiac Morphogens Drive Adult Csc Commitment In Bona-fide Cardiomyocytesmentioning

confidence: 99%

Molecular basis of functional myogenic specification ofBona Fidemultipotent adult cardiac stem cells

et al. 2018

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“…Unlike DNA sequences, largely the same in every cell, epigenomic changes can occur because of dietary, behavioural and other environmental exposures, including physical and psychological stressors [7,8]. Abnormalities in DNA methylation are associated with many diseases and typically manifest through inappropriate gene expression [9]. Through comparative analysis of methylome data, we can attain a clearer understanding of the molecular mechanisms that underlie pathology in different population subsets.…”

Section: Introductionmentioning

confidence: 99%

Using NGS-methylation profiling to understand the molecular pathogenesis of young MI patients who have subsequent cardiac events

Thunders

Holley

Harding³

et al. 2019

Epigenetics

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Globally, ischaemic heart disease is a major contributor to premature morbidity and mortality. A significant number of young Myocardial Infarction (MI) patients (aged <55 y) have subsequent cardiac events within a year of their index event. This study used Next Generation Sequencing (NGS) methylation to understand the pathogenesis in this subset of young MI patients, comparing them to a cohort of patients without recurrent events. Cases and controls were matched for age, gender, ethnicity, and comorbidities. Differential methylation analyses were performed on Reduced Representation Bisulphite Sequencing (RRBS) data. Across the group and within case-control pairs' variation were analysed. Pairwise comparisons across each matched case-control pair resulted in a list of genes that were consistently significantly differentially methylated between all 16 matched pairs. This gene list was input into pathway analysis databases. Of particular relevance to cardiac pathology the following pathways were identified as over-represented in the patients with recurrent events; cell adhesion, transcription regulation and cardiac electrical conduction, specifically relating to calcium channel activity. This study looked at methylation differences between two populations of young MI patients. There were significantly different methylation profiles between the two groups studied; key pathways were identified as specifically affected in the patients with recurrent cardiac events. Matched pairwise comparisons and detailed interpretations of DNA methylation data may help to elucidate complex pathogeneses within and between clinical subtypes. Further analysis will determine whether these epigenomic differences can be useful as predictive biomarkers of clinical progression.

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Epigenetics of the failing heart

Marı́n-Garcı́a

Akhmedov

2015

Heart Fail Rev

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With the impressive advancement in high-throughput 'omics' technologies over the past two decades, epigenetic mechanisms have emerged as the regulatory interface between the genome and environmental factors. These mechanisms include DNA methylation, histone modifications, ATP-dependent chromatin remodeling and RNA-based mechanisms. Their highly interdependent and coordinated action modulates the chromatin structure controlling access of the transcription machinery and thereby regulating expression of target genes. Given the rather limited proliferative capability of human cardiomyocytes, epigenetic regulation appears to play a particularly important role in the myocardium. The highly dynamic nature of the epigenome allows the heart to adapt to environmental challenges and to respond quickly and properly to cardiac stress. It is now becoming evident that histone-modifying and chromatin-remodeling enzymes as well as numerous non-coding RNAs play critical roles in cardiac development and function, while their dysregulation contributes to the onset and development of pathological cardiac remodeling culminating in HF. This review focuses on up-to-date knowledge about the epigenetic mechanisms and highlights their emerging role in the healthy and failing heart. Uncovering the determinants of epigenetic regulation holds great promise to accelerate the development of successful new diagnostic and therapeutic strategies in human cardiac disease.

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Epigenetic regulation and heart failure

Cited by 7 publications

References 120 publications

Molecular basis of functional myogenic specification ofBona Fidemultipotent adult cardiac stem cells

Molecular basis of functional myogenic specification ofBona Fidemultipotent adult cardiac stem cells

Using NGS-methylation profiling to understand the molecular pathogenesis of young MI patients who have subsequent cardiac events

Epigenetics of the failing heart

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