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Special Issue "Improvement of Cardiac Function in Heart Failure 2017"

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 January 2017)

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Special Issue Editors

Guest Editor Prof. Dr. H.W.M. Niessen Department of Pathology, VU University Medical Centre, Room 0E46, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands E-Mail Fax: +31 20 444 2964 Interests: cardiovascular inflammation
Guest Editor Dr. Paul A.J. Krijnen Department of Pathology, VU University Medical Centre, Room 0E46, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands E-Mail Phone: +31 20 444 4003 Fax: +31 20 444 2964 Interests: cardiovascular inflammation

Special Issue Information

Dear Colleagues,

Heart Failure is a complex syndrome with multiple causes and is responsible for high morbidity and mortality worldwide, especially in the elderly. The prognosis of heart failure patients remains poor, despite recent advances in the management of heart failure. Therefore, there is a need for new treatment strategies improving the clinical outcomes, such as therapies targeting cellular mechanisms of heart failure including inflammatory processes, oxidative stress, as well as abnormalities in perfusion, molecular mechanisms, electrical conduction, autoimmunity and ventricular remodeling.

This special issue discusses not only the pathophysiology of heart failure but also biomarker and therapy development to improve cardiac function in heart failure.

Prof. Dr. H.W.M. Niessen
Dr. Paul A.J. Krijnen
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

heart failure
myocardial infarction
myocarditis
animal models
clinical trial
inflammation
stem cells
biomarker development
heart failure therapy
diagnostic imaging
immunohistochemistry
metabolics
molecular diagnostics
proteomics
personalized medicine
cardiomyocyte contractility
mutations in contractile proteins
coronary microcirculation
fibrosis
arrhythmia
hypertrophy
autoimmunity
oxidative stress
angio/arteriogenesis
cardiac perfusion

Related Special Issue

Improvement of Cardiac Function in Heart Failure in International Journal of Molecular Sciences (13 articles)

Published Papers (5 papers)

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Research

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Open AccessArticle Clinical Correlates and Prognostic Value of Plasma Galectin-3 Levels in Degenerative Aortic Stenosis: A Single-Center Prospective Study of Patients Referred for Invasive Treatment

by Beata Bobrowska, Ewa Wieczorek-Surdacka, Olga Kruszelnicka, Bernadeta Chyrchel, Andrzej Surdacki and Dariusz Dudek

Int. J. Mol. Sci. 2017, 18(5), 947; doi:10.3390/ijms18050947

Received: 31 January 2017 / Revised: 24 March 2017 / Accepted: 25 April 2017 / Published: 29 April 2017

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Abstract

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Galectin-3 (Gal-3), a β-galactoside-binding lectin, has been implicated in myocardial fibrosis, development of left ventricular (LV) dysfunction and transition from compensated LV hypertrophy to overt heart failure (HF), being a novel prognostic marker in HF. Risk stratification is crucial for the choice of the optimal therapy in degenerative aortic stenosis (AS), affecting elderly subjects with coexistent diseases. Our aim was to assess correlates and prognostic value of circulating Gal-3 in real-world patients with degenerative AS referred for invasive treatment. Gal-3 levels were measured at admission in 80 consecutive patients with symptomatic degenerative AS (mean age: 79 ± 8 years; aortic valve area (AVA) index: 0.4 ± 0.1 cm²/m²). The therapeutic strategy was chosen following a dedicated multidisciplinary team-oriented approach, including surgical valve replacement (n = 11), transcatheter valve implantation (n = 19), balloon aortic valvuloplasty (BAV) (n = 25) and optimal medical therapy (n = 25). Besides routine echocardiographic indices, valvulo-arterial impedance (Zva), an index of global LV afterload, was computed. There were 22 deaths over a median follow-up of 523 days. Baseline Gal-3 correlated negatively with estimated glomerular filtration rate (eGFR) (r = −0.61, p < 0.001) and was unrelated to age, symptomatic status, AVA index, LV ejection fraction, LV mass index or Zva. For the study group as a whole, Gal-3 tended to predict mortality (Gal-3 >17.8 vs. Gal-3 <17.8 ng/mL; hazard ratio (HR): 2.03 (95% confidence interval, 0.88–4.69), p = 0.09), which was abolished upon adjustment for eGFR (HR: 1.70 (0.61–4.73), p = 0.3). However, in post-BAV patients multivariate-adjusted pre-procedural Gal-3 was associated with worse survival (HR: 7.41 (1.52–36.1), p = 0.01) regardless of eGFR. In conclusion, the inverse eGFR–Gal-3 relationship underlies a weak association between Gal-3 and adverse outcome in patients with degenerative AS referred for invasive therapy irrespective of type of treatment employed. In contrast, pre-procedural Gal-3 appears an independent mortality predictor in high-risk AS patients undergoing BAV. Full article

(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure 2017)

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Open AccessArticle Myocardial Ischemic Postconditioning Promotes Autophagy against Ischemia Reperfusion Injury via the Activation of the nNOS/AMPK/mTOR Pathway

by Maojuan Hao, Suhua Zhu, Liang Hu, Hongyi Zhu, Xiaowei Wu and Qingping Li

Int. J. Mol. Sci. 2017, 18(3), 614; doi:10.3390/ijms18030614

Received: 9 January 2017 / Revised: 27 February 2017 / Accepted: 7 March 2017 / Published: 11 March 2017

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Autophagy participates in the progression of many diseases, comprising ischemia/ reperfusion (I/R). It is reported that it is involved in the protective mechanism of ischemic postconditioning (IPostC). According to research, neuronal nitric oxide synthase (nNOS) is also involved in the condition of I/R and IPostC. However, the relationship between nNOS, autophagy and IPostC has not been previously investigated. We hypothesize that IPostC promotes autophagy activity against I/R injury partially through nNOS-mediated pathways. Mouse hearts were subjected to I/R injury through the ligation of the left anterior descending coronary artery. H9c2 cells were subjected to hypoxia/reoxygenation (H/R) in vitro. IPostC, compared with I/R, restored nNOS activity, increased the formation of autophagosome and restored the impaired autophagic flux, thus autophagic activity was raised markedly. IPostC increased adenosine monophosphate-activated protein kinase (AMPK) phosphorylation and suppressed mammalian target of rapamycin (mTOR), but a selective nNOS inhibitor abolished those effects. Similar effects of IPostC were demonstrated in H9c2 cells in vitro. IPostC decreased infarct size and preserved most of the normal structure. The level of reactive oxygen species (ROS) and cell apoptosis were reduced by IPostC with improved cell viability and mitochondrial membrane potential. However, an autophagy inhibitor suppressed the protective effects. These results suggest that IPostC promoted autophagy against I/R injury at least partially via the activation of nNOS/AMPK/mTOR pathway. Full article

(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure 2017)

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Open AccessArticle Effects of the Activin A–Follistatin System on Myocardial Cell Apoptosis through the Endoplasmic Reticulum Stress Pathway in Heart Failure

by Miao Liu, Cuiying Mao, Jiayu Li, Fanglei Han and Ping Yang

Int. J. Mol. Sci. 2017, 18(2), 374; doi:10.3390/ijms18020374

Received: 23 November 2016 / Revised: 26 January 2017 / Accepted: 31 January 2017 / Published: 10 February 2017

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Background: A previous study suggested that activin A inhibited myocardial cell apoptosis. This study thus aimed to explore the effects of the activin A–follistatin system on myocardial cell apoptosis in heart failure (HF) rats in order to determine whether or not the mechanism operates through the endoplasmic reticulum stress (ERS) pathway. Methods: Myocardial infarction (MI) by vascular deprivation was used to induce HF. The enzyme-linked immunosorbent assay was used to detect activin A, follistatin and brain natriuretic peptide (BNP) contents in serum. Immunohistochemical staining for activin A, follistatin, CCAAT-enhancer-binding protein (C/EBP) homologous protein (CHOP) and caspase-3 was performed on the myocardial tissue. The activin A-stimulated apoptosis of H9c2 cells was tested by flow cytometry. Western blot was used to detect the expression levels of activin A, follistatin and ERS-related proteins. Results: It was found that the high expression of activin A could cause activin A–follistatin system imbalance, inducing myocardial cell apoptosis via ERS in vivo. When HF developed to a certain stage, the expression of follistatin was upregulated to antagonize the expression of activin A. Activin A inhibited cardiomyocyte apoptosis with a low concentration and promoted apoptosis with a high concentration in vitro, also via ERS. Conclusion: Activin A–follistatin system participated in ERS-mediated myocardial cell apoptosis in HF. Full article

(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure 2017)

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Open AccessArticle T-Tubular Electrical Defects Contribute to Blunted β-Adrenergic Response in Heart Failure

by Claudia Crocini, Raffaele Coppini, Cecilia Ferrantini, Ping Yan, Leslie M. Loew, Corrado Poggesi, Elisabetta Cerbai, Francesco S. Pavone and Leonardo Sacconi

Int. J. Mol. Sci. 2016, 17(9), 1471; doi:10.3390/ijms17091471

Received: 12 July 2016 / Revised: 17 August 2016 / Accepted: 30 August 2016 / Published: 3 September 2016

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Alterations of the β-adrenergic signalling, structural remodelling, and electrical failure of T-tubules are hallmarks of heart failure (HF). Here, we assess the effect of β-adrenoceptor activation on local Ca²⁺ release in electrically coupled and uncoupled T-tubules in ventricular myocytes from HF rats. We employ an ultrafast random access multi-photon (RAMP) microscope to simultaneously record action potentials and Ca²⁺ transients from multiple T-tubules in ventricular cardiomyocytes from a HF rat model of coronary ligation compared to sham-operated rats as a control. We confirmed that β-adrenergic stimulation increases the frequency of Ca²⁺ sparks, reduces Ca²⁺ transient variability, and hastens the decay of Ca²⁺ transients: all these effects are similarly exerted by β-adrenergic stimulation in control and HF cardiomyocytes. Conversely, β-adrenergic stimulation in HF cells accelerates a Ca²⁺ rise exclusively in the proximity of T-tubules that regularly conduct the action potential. The delayed Ca²⁺ rise found at T-tubules that fail to conduct the action potential is instead not affected by β-adrenergic signalling. Taken together, these findings indicate that HF cells globally respond to β-adrenergic stimulation, except at T-tubules that fail to conduct action potentials, where the blunted effect of the β-adrenergic signalling may be directly caused by the lack of electrical activity. Full article

(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure 2017)

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Review

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Open AccessReview Targeting the Innate Immune Response to Improve Cardiac Graft Recovery after Heart Transplantation: Implications for the Donation after Cardiac Death

by Stefano Toldo, Mohammed Quader, Fadi N. Salloum, Eleonora Mezzaroma and Antonio Abbate

Int. J. Mol. Sci. 2016, 17(6), 958; doi:10.3390/ijms17060958

Received: 5 April 2016 / Revised: 30 May 2016 / Accepted: 1 June 2016 / Published: 17 June 2016

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Heart transplantation (HTx) is the ultimate treatment for end-stage heart failure. The number of patients on waiting lists for heart transplants, however, is much higher than the number of available organs. The shortage of donor hearts is a serious concern since the population affected by heart failure is constantly increasing. Furthermore, the long-term success of HTx poses some challenges despite the improvement in the management of the short-term complications and in the methods to limit graft rejection. Myocardial injury occurs during transplantation. Injury initiated in the donor as result of brain or cardiac death is exacerbated by organ procurement and storage, and is ultimately amplified by reperfusion injury at the time of transplantation. The innate immune system is a mechanism of first-line defense against pathogens and cell injury. Innate immunity is activated during myocardial injury and produces deleterious effects on the heart structure and function. Here, we briefly discuss the role of the innate immunity in the initiation of myocardial injury, with particular focus on the Toll-like receptors and inflammasome, and how to potentially expand the donor population by targeting the innate immune response. Full article

(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure 2017)

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