Epigenetics in heart failure phenotypes

2017

Biomed. Res. Ther.

Heart failure (HF) is considered a leading cause of death in patients with established cardiovascular (CV) and metabolic diseases. Although current treatment strategy has improved survival rate and clinical outcomes of HF, the HF prevalence exhibits growth especially in older patients' population and survivors after coronary atherothrombotic events. Current clinical guidelines regarding treatment and prevention of HF claim the role of biological markers as pretty easy and powerful tool for diagnosis, risk stratification, and prognostication of HF. However, there is not clear whether all these biological markers are able to equally predict CV death and HF-related outcomes in patients with acute and chronic HF as well as in various phenotypes of HF. The aim of the review is to discuss a role of in risk stratification and individual treatment in patients with different phenotypes of HF.

Section: Endothelial Cell-derived Micro Particles and Endothelial Promentioning

confidence: 99%

Up-to-date clinical approaches of biomarkers’ use in heart failure

2017

Biomed. Res. Ther.

“…Whether similar effects trigger structure and functional abnormality in cell precursors that involve in the pathogenesis of HF is not well established, although accumulation of reactive oxygen species leading to the swelling and fragmentation of mitochondria of EPCs has now described as factor of decreased repair ability of precursors [23]. Indeed, enhancement of oxidative stress and mitochondrial dysfunction of EPCs may negatively effect of number and function of ones (mobbing, proliferation, regeneration, apoptosis, differentiation, cell-cell interaction, survival) through intracellular signaling pathways (Akt/nitric oxide, PI3K/nitric oxide), which may operate in signal-regulated kinase and the inflammatory genes expression, such as interleukin-6 and TNF-α, and synthesis of specific miRNAs (-126, -128, -130) [24,25]. Finally, epigenetically modified EPCs are not able to maintain the homeostasis of vasculature and trigger inadequate endothelial responses that realize ED and microvascular inflammation.…”

Section: Epc Dysfunction As a Central Player In Hf Risk Developmentmentioning

confidence: 99%

Progenitor Cell Dysfunction: The Role of Endothelial Precursors in Heart Failure

2017

J Biomedical Sci

Heart failure (HF) a leading cause of premature death in patients with established cardiovascular (CV) disease. Although the global burden of HF is increasing, there is no evidence regarding promising results that improves longterm clinical outcomes especially for HF with preserved and mid-regional pump function. In this context, determination of the vulnerable populations at higher risk of HF development and progression is very promising. Endothelial dysfunction (ED) plays a central role in the manifestation of HF regardless its phenotypes. There is a large body of evidence regarding that the endothelial progenitor cells (EPCs) as a component of endogenous vascular repair system could be modified by several stimuli including epigenetic factors and thereby they are involved in the pathogenesis of ED. However, there is unclear whether EPC dysfunction is only whiteness of HF or it could be a factor of HF manifestation in vulnerable population. The short communication is depicted the uncertain role of EPC dysfunction in pathogenesis of HF.

“…Another way that could probably explain the role of uric acid in pathogenesis of HF relates to an ability of uric acid to epigenetically regulate a survival of endothelial precursors, mediate their mobbing and differentiation, as well as coordinate a turn-over effect of metabolic memory into repair capability of cell precursors [19,20]. Indeed, SUA levels independently and inversely associated with number of circulating endothelial progenitor cells in HF individuals [21].…”

Section: Short Communicationmentioning

confidence: 99%

Serum uric acid as a metabolic regulator of endothelial function in heart failure

2017

Arch Clin Hypertens

Citation: Berezin AE (2017) Serum uric acid as a metabolic regulator of endothelial function in heart failure. Arch Clin Hypertens 3(1): 027-029. DOI: http://dx.doi.org/10.17352/ach.000016 AbstractThe development of heart failure (HF) associated with elevated level of serum uric acid (SUA). Additionally, the majority of individuals with traditional cardiovascular risk factors contributing in HF risk exhibited increased levels of SUA. Although SUA lowering drugs are widely used in patients with symptomatic hyperuricemia and gout beyond their etiologies, there is no agreement of SUA below target level 6.0 mg/dL in asymptomatic individuals with kidney injury and CV disease and data of ones in heart failure (HF) are suffi ciently controversial. First SUA plays an important role in inducing oxidative stress, infl ammation, neurohumoral activation, and endothelial dysfunction. Secondary, SUA may act as antioxidant contributing in restoring of vascular function. Moreover, SUA is able to epigenetically regulate a survival of endothelial precursors, mediate their mobbing and differentiation, as well as coordinate a turn-over effect of metabolic memory phenomenon into repair capability of cell precursors. However, elevated SUA level was found a predictor of adverse clinical outcomes of HF. The short communication is depicted the importance of new clinical data to confi rm the emerging reparative ability of SUA in HF and its role as promising target for treatment in cardiac failure. Short Communication Serum uric acid as a metabolic regulator of endothelial function in heart failureAlexander E Berezin* Short CommunicationThere is a large body of evidence regarding the role of serum uric acid (SUA) in pathogenesis of cardiovascular diseases (CVD) including heart failure (HF). Although SUA levels above the current international reference limit equal 6.0 mg/dL are highly prevalent in chronic kidney disease (CKD), hyperuricemia strongly associates with in-hospital CV mortality independently from CKD etiology and renal function in individuals admitted to the hospital due to several causes, i.e. acute myocardial infarction, stroke, hypertensive emergencies, acute / chronic heart failure, arrhythmia, shock and sepsis.In contrast, hypouricemia did not associate with increased mortality rate in patient populations with established CVD [1]. In HF an elevated SUA level was found due to several mechanisms including an increased activity of xanthine oxidase (XO), which is a key enzyme in uric acid synthesis and is under control of infl ammatory cytokines / chemokines, some growth factors, and intermediates (blood glucose). Whether SUA could be an independent predictor of HF development is not fully clear. Recent clinical studies and some meta-analysis have shown that elevated SUA levels were associated with an increased risk of incident HF, observed in majority of patients with established chronic HF and relate to adverse clinical outcomes in HF [8][9][10][11]. However, the impact of uric acid on all-cause mortality and HF-related dea...