Progenitor Endothelial Cell Dysfunction in Heart Failure: Clinical Implication and Therapeutic Target?

Berezin, Alexander E.

doi:10.4172/2161-1025.1000176

Cited by 7 publications

(6 citation statements)

References 32 publications

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“…However, no epigenetically active drugs that have actually entered clinical trials for HFpHF and HFrEF have been approved by the FDA [107] . Yet, there is uncertainty regarding perspectives of therapeutic strategy based on the inhibition of cardiac hypertrophy in clinical settings [108] , [109] .…”

Section: Future Direction: Epigenetic-based Therapies Of Heart Failurmentioning

confidence: 99%

Epigenetics in heart failure phenotypes

Berezin

2016

BBA Clinical

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Chronic heart failure (HF) is a leading clinical and public problem posing a higher risk of morbidity and mortality in different populations. HF appears to be in both phenotypic forms: HF with reduced left ventricular ejection fraction (HFrEF) and HF with preserved left ventricular ejection fraction (HFpEF). Although both HF phenotypes can be distinguished through clinical features, co-morbidity status, prediction score, and treatment, the clinical outcomes in patients with HFrEF and HFpEF are similar. In this context, investigation of various molecular and cellular mechanisms leading to the development and progression of both HF phenotypes is very important. There is emerging evidence that epigenetic regulation may have a clue in the pathogenesis of HF. This review represents current available evidence regarding the implication of epigenetic modifications in the development of different HF phenotypes and perspectives of epigenetic-based therapies of HF.

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Section: Future Direction: Epigenetic-based Therapies Of Heart Failurmentioning

confidence: 99%

Epigenetics in heart failure phenotypes

Berezin

2016

BBA Clinical

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“…This effect is mediated by increased expression of angiogenic genes (NOTCH1, cadherin-5, sirtuins, and angiopoietin-like-2), and decreased expression of progenitor cell marker genes (CD133, CXCR4, and C-KIT) [23][24][25]. Although DNA and histone methylation lead to distinguished repression of heterochromatin (stable long-term repression and local formation, respectively) [26], the crosstalk between SET domain histone methyltransferases and DNA methyltransferases is essential for relationship of both epigenetic pathways, which mediate reprogramming of EPCs in DM [27].…”

Section: Editorialmentioning

confidence: 99%

Epigenetic Mechanisms of Endothelial Progenitor Cell Dysfunction

Berezin¹

2016

J Clin Epigenet

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Diabetes mellitus remains a leading factor contributing increased morbidity and mortality worldwide. The development and progression of DM associates with microvascular and macrovascular complications linked the DM with cardiovascular events. The impaired ability of endothelium to repair the injury and restore integrity depends in part on number and function of endothelial progenitor cells (EPCs). The mechanisms underlying EPC dysfunction in DM predominantly include weak bone marrow mobilization, decreased proliferation, and shortened survival. The weak function and lowered number of EPCs obtained from peripheral blood were recently found in 1 type and 2 type of DM. It has suggested that glucose toxicity, lipid toxicity, inflammation and oxidative stress may directly and indirectly via several molecular mechanisms worse of EPCs function and, however, lead to deficiency of circulating angiopoetic progenitors. Epigenetic changes are considered important key to understand whether EPCs dysfunction is reversible setting or not. The aim of editorial is to discuss around the role of epigenetic changes in EPCs in linking of DM with cardiovascular risk. Keywords: Diabetes mellitus; Endothelial progenitor cells; Endothelial dysfunction; Endothelial injury; Impaired vascular reparation; Cardiovascular risk EditorialDiabetes mellitus (DM) is a major metabolic factor leading to increased mortality and morbidity associated with higher incidence of disability, huge social and economic burden [1,2]. Recent basic and clinical studies have shown that development and progression of DM has impaired endothelium structure and integrity via several molecular mechanisms induced by glucose toxicity, lipid toxicity, oxidative stress, and inflammation [3][4][5][6]. On this way, epigenetic changes affected function and structure of endothelial-derived progenitor cells (EPCs) might lead to worsening of endothelium reparation [7]. Moreover, the EPCs dysfunction might be a clue in the initiation of DM-related microvascular and macrovascular complications [8,9] having a great predictive value [9].EPCs originated from bone marrow cells and peripheral blood cells support endothelial homoeostasis and attenuate angiogenesis. The mechanisms underlying EPC dysfunction in DM predominantly include weak bone marrow mobilization, decreased proliferation, and shortened survival [10]. Importantly, the deregulation of epigenetic features of EPCs plays a key role in DM-induced vascular injury and endothelial dysfunction [11]. DNA methylation / hydroxymethylation / transmethylation, histone modifications, and differential expression of specific non-coding RNAs like microRNA (miRNAs) are discussed as causative mechanisms of epigenetic modifications [12]. Despite this, the early phases of epigenetically changes in EPCs are pre-diabetic situation affected mitochondrial injury upon hyperglycemic insult, oxidative stress activation, and lowering survival ability of cell organelles [13]. Indeed, lowered cell membrane protection against hyperglycemic endoth...

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“…Because uncommitted progenitor cells can differentiate toward the several phenotypes (i.e. endothelial cell phenotype), it is possible that a broader derangement of immature EPCs predisposes to CV complications in DM [69]. Whether weak functionality and / or lower number of EPCs exist prior to both CV risk and established CV / metabolic diseases or they appear resulting in CV risk factors' influence on epigenetic mechanisms of immature progenitors is not fully clear.…”

Section: The Concept Of Impaired Cardiac and Vessel Reparation In Diamentioning

confidence: 99%

Endothelial Progenitor Cells Dysfunction in Diabetes Mellitus

2016

ARC Journal of Diabetes and Endocrinology

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Progenitor Endothelial Cell Dysfunction in Heart Failure: Clinical Implication and Therapeutic Target?

Cited by 7 publications

References 32 publications

Epigenetics in heart failure phenotypes

Epigenetics in heart failure phenotypes

Epigenetic Mechanisms of Endothelial Progenitor Cell Dysfunction

Endothelial Progenitor Cells Dysfunction in Diabetes Mellitus

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