Recent Developments in Heart Failure

Dassanayaka, Sujith; Jones, Steven P.

doi:10.1161/circresaha.115.305765

Cited by 83 publications

(61 citation statements)

References 88 publications

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“…Heart failure (HF) is a common complication of myocardial infarction (MI) that leads to high mortality worldwide (1,24,30). Cardiac remodeling is a major pathological change in the development of post-MI HF (4,22), and cardiomyocyte injury and cardiac fibrosis are two main mechanisms in the process of cardiac remodeling (3,11). Cardiac fibrosis is a complex and elaborate pathological process affected by multiple factors (13,27), yet the molecular mechanisms involved in the pathogenesis of cardiac fibrosis are still incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

BMI1 promotes cardiac fibrosis in ischemia-induced heart failure via the PTEN-PI3K/Akt-mTOR signaling pathway

Yang

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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Cardiac fibrosis has been known to play an important role in the etiology of heart failure after myocardial infarction (MI). B lymphoma Mo-MLV insertion region 1 homolog (BMI1), a transcriptional repressor, is important for fibrogenesis in the kidneys. However, the effect of BMI1 on ischemia-induced cardiac fibrosis remains unclear. BMI1 was strongly expressed in the infarct region 1 wk post-MI in mice and was detected by Western blot and histological analyses. Lentivirus-mediated overexpression of BMI1 significantly promoted cardiac fibrosis, worsened cardiac function 4 wk after the intervention in vivo, and enhanced the proliferation and migration capabilities of fibroblasts in vitro , whereas downregulation of BMI1 decreased cardiac fibrosis and prevented cardiac dysfunction in mice 4 wk post-MI in vivo. Furthermore, upregulated BMI1 inhibited phosphatase and tensin homolog (PTEN) expression, enhanced phosphatidylinositol 3-kinase (PI3K) expression, and increased the phosphorylation level of Akt and mammalian target of rapamycin (mTOR) in mice 4 wk after lentiviral infection, which was in accordance with the changes seen in their infarcted myocardial tissues. At the same time, the effects of BMI1 on cardiac fibroblasts were reversed in vitro when these cells were exposed to NVP-BEZ235, a dual-kinase (PI3K/mTOR) inhibitor. In conclusion, BMI1 is associated with cardiac fibrosis and dysfunction after MI by regulating cardiac fibroblast proliferation and migration, and these effects could be partially explained by the regulation of the PTEN-PI3K/Akt-mTOR pathway. NEW & NOTEWORTHY Ischemia-induced B lymphoma Mo-MLV insertion region 1 homolog (BMI1) significantly promoted cardiac fibrosis and worsened cardiac function in vivo, whereas downregulation of BMI1 decreased cardiac fibrosis and prevented cardiac dysfunction in myocardial infarcted mice. BMI1 also enhanced proliferation and migration capabilities of fibroblasts in vitro; these effects were reversed by NVP-BEZ235. Effects of BMI1 on cardiac fibrosis could be partially explained by regulation of the phosphatase and tensin homolog-phosphatidylinositol 3-kinase/Akt-mammalian target of rapamycin pathway.

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Section: Introductionmentioning

confidence: 99%

BMI1 promotes cardiac fibrosis in ischemia-induced heart failure via the PTEN-PI3K/Akt-mTOR signaling pathway

Yang

et al. 2019

American Journal of Physiology-Heart and Circulatory Physiology

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“…1 Heart Failure (HF) is a clinical syndrome caused by structural and functional defects in myocardium resulting in impairment of ventricular filling or the ejection of blood. 2 Unlike western countries where heart failure is predominantly a disease of elderly, in Among the unfavorable epigenetic factors in relation to CVDs, vitamin D deficiency was found to be an important modifiable factor with the treatment where low levels of 25-hydroxyvitamin D were related to low birth weight, prematurity, increased perinatal mortality, and decreased glucose tolerance leading to unfavorable renal and cardiovascular outcomes in adulthood. 6 Although the best-characterized sequelae of vitamin D deficiency involve the musculoskeletal system, a growing body of evidence suggests that low levels of vitamin D may adversely affect the cardiovascular system.…”

Section: Introductionmentioning

confidence: 99%

Study to determine serum vitamin D levels in patients with congestive heart failure

et al. 2019

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Background: It was to evaluate the association of serum levels of vitamin D in patients with congestive heart failure.Methods: The present study was conducted in the department of Medicine at Chattrapati Shivaji Subharti Hospital among 100 patients, aged 18 years and above diagnosed as congestive heart failure on the basis of clinical and echocardiographic evidence. Clinical manifestations looked for CHF were: Dyspnea, orthopnea, acute pulmonary edema, cerebral symptoms, cheyne-stokes respiration, cyanosis, sinus tachycardia, raised jugular venous pressure, congestive hepatomegaly and pedal edema. In the present study deficiency/ insufficiency of vitamin D was considered when the presence of levels of 25-hydroxyvitamin D was <30 ng/ml. Laboratory tests performed to diagnose congestive heart failure and serum vitamin D levels were complete blood count, KFT (urea, serum creatinine), serum electrolytes, ECG, chest X ray and echocardiogram. Data were tabulated and examined using the statistical package for Social Sciences Version 22.0.Results: When data was assessed for comparison in relation to NHYA grades and vitamin D levels, it was found to be statistically significant. The Mean±SD scores of serum urea (mg/dL) was found to be 44.7±56.4, 47.3±63.8 and 36.4± 18.3 in whole study sample, vitamin D levels <30 and vitamin D levels >30 respectively with statistically significant difference. The Mean±SD scores of CPK MB (IU/L) was found to be 33.1±20.8 and 18.6±13.3 among the subjects having vitamin D levels <30 and vitamin D levels >30 respectively with statistically significant difference.Conclusions: The results of the present study suggest that low levels of vitamin D may adversely affect the cardiovascular system.

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“…This clinical syndrome is mostly seen in the people of age 65 or more and is related to the mortality and morbidity. 2 The problem arises most often in the left ventricle because it is the left ventricle that acts as main pumping chamber and pumps the oxygenated blood all over the body. This generally becomes the reason of its impairment than any other chambers of the heart, and this failure in which the left ventricle functions get impaired is called as left-sided heart failure or left ventricular heart failure.…”

Section: Introductionmentioning

confidence: 99%

Nebivolol: An Appealing, Awaited and Nitric Oxide Potentiator Drug for the Treatment of Heart Failure

Saini¹,

Wal²,

Verma³

et al. 2018

JYP

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Nebivolol is a third generation beta-blocker that possesses the highest selectivity for beta-1 receptors than beta-2 receptors than any other beta blocker in its class. Long-term therapy of nebivolol, in clinical trials, has been found to be very effective in increasing the left ventricular ejection fraction, reducing all-cause mortality, and reducing the New York Heart Association (NYHA) class of heart failure. The novelty of nebivolol exists in its unique nitric oxide potentiating effects in the myocardial and endothelial cells by the activation of beta-3 adrenergic receptors by which it produces most of its actions. It produces many useful effects and helps to abate the disease progression and prolongs the survival. In many clinical studies, it has been found to be safe and well tolerated. A literature search was made on PubMed database with the keywords: "Heart failure" , "Nebivolol" , and "beta-blocker" . A total of 176 articles were found and were the combination of review articles and research articles. A further selection of articles was made by the exclusion of non-relevant articles to achieve the objective of this review. It is approved for the treatment of hypertension in the United States and is under review by the federal agency, United States Food and Drugs Administration for the treatment of heart failure. This article sole intention is to review all the clinically important aspects of nebivolol on the basis of which nebivolol can be definitely considered for its inclusion in the drug therapy list for heart failure which will ease the individualization of drug therapy. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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Recent Developments in Heart Failure

Cited by 83 publications

References 88 publications

BMI1 promotes cardiac fibrosis in ischemia-induced heart failure via the PTEN-PI3K/Akt-mTOR signaling pathway

BMI1 promotes cardiac fibrosis in ischemia-induced heart failure via the PTEN-PI3K/Akt-mTOR signaling pathway

Study to determine serum vitamin D levels in patients with congestive heart failure

Nebivolol: An Appealing, Awaited and Nitric Oxide Potentiator Drug for the Treatment of Heart Failure

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