Research Emeline Van Craenenbroeck

Abstract

Doxorubicin (DOX) is a widely used and highly effective chemotherapeutic agent with severe side effects, affecting the quality of life of cancer patients and survivors. DOX-induced skeletal muscle toxicity, especially muscle wasting and dysfunction, is of particular concern as it increases morbidity and mortality rates. In the current proposal, we aim to investigate the role of myokines and miRNAs within the mechanisms of DOX-induced skeletal muscle wasting through an in vitro (C2C12 cell line) and in vivo (mice) model. Identification of these myokines and miRNAs, that are expressed and exert their action in skeletal muscle, offer a novel theoretical basis to unravel the underlying cellular and molecular mechanisms and provide novel insights in the diagnosis and treatment of skeletal muscle wasting following DOX-treatment. We hypothesize that myokines and miRNAs play a crucial role in the pathogenesis of DOX-induced skeletal muscle wasting. In addition, we will study the potential cellular and molecular counteracting effects of muscle contraction on muscle wasting by 1) electrical pulse stimulation on DOX-treated C2C12 cells and 2) single exercise bouts in mice immediately before each DOX-cycle. We hypothesize that exercise is a feasible strategy in clinical practice to prevent DOX-induced muscle wasting. Finally, to improve clinical translatability we will also study the therapeutic use of single exercise bouts in a murine cancer cachexia model treated with DOX.

Researcher(s)

• Promoter: van Breda Eric
• Co-promoter: Guns Pieter-Jan
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Van Asbroeck Birgit

Research team(s)

• Movement Antwerp (MOVANT)

Project type(s)

• Research Project

Abstract

The Vevo LAZR-X is an imaging platform for preclinical applications capable of acquiring in vivo anatomical, functional and molecular data. It combines ultra high frequency ultrasound with photoacoustic imaging (a new biomedical imaging modality based on the use of lasergenerated ultrasound) for high resolution images as well as software for analysis and quantification. This equipment will be used in the context of the study of (cardio)vascular diseases, genetics of the heart, heart valves and aortic dissection, kidney diseases and their effects on the heart and blood vessels, and for cancer research.

Researcher(s)

• Promoter: De Meyer Guido
• Co-promoter: De Keulenaer Gilles
• Co-promoter: Heidbuchel Hein
• Co-promoter: Loeys Bart
• Co-promoter: Smits Evelien
• Co-promoter: Van Craenenbroeck Emeline
• Co-promoter: Verhulst Anja
• Co-promoter: Verstraeten Aline

Research team(s)

• Physiopharmacology (PHYSPHAR)

Project type(s)

• Research Project

Abstract

Adults with a congenital heart disease (ACHD) have a lower functional capacity, reduced quality of life and worse prognosis compared to healthy individuals. ACHD and patients with heart failure (HF) induced by other aetiologies share many characteristics, incl. exercise intolerance, right ventricular (RV) dysfunction and increased inflammatory cytokine levels. Among the pathophysiological changes in HF, endothelial dysfunction is highlighted. However, the presence of endothelial dysfunction in ACHD is unknown as literature is limited and conflicting. I hypothesize that coronary microvascular dysfunction (CMD) is important in the pathophysiology of ACHD. I believe that multiple factors incl. genetics, underlying cardiac abnormality, history of cardiac surgery and RV overload, further aggravated by classical acquired risk factors (including overweight, hypertension and sedentary lifestyle), alter shear stress and promote systemic inflammation and endothelial oxidative stress in ACHD leading to a reduced nitric oxide bioavailability and endothelial dysfunction. As such I assume that CMD is associated with systemic endothelial dysfunction, reflecting CMD as part of a systemic microvascular disorder. I am convinced that detecting CMD is important to allow identification of ACHD with an unfavorable prognosis and that this CMD can easily be identified with adenosine-based Doppler echocardiography. Finally, the potential therapeutic effect of exercise training will be investigated.

Researcher(s)

• Promoter: Van Berendoncks An
• Co-promoter: Hens Wendy
• Co-promoter: Segers Vincent
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Vanreusel Inne

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Mitral valve prolapse (MVP) is a valvular disorder with a prevalence of 2-3% in the general population. MVP can be associated with mitral regurgitation (MR), congestive heart failure, ventricular arrhythmias and sudden cardiac death. Barlow's Disease (BD) and Fibro-Elastic deficiency (FED) present the 2 most common MVP phenotypes. In recent years, several genetic mutations have been identified which might play a role in the pathophysiology of MVP, but the exact genotype-phenotype correlation remains largely unknown. Furthermore, recent evidence points to the existence of a concomitant cardiomyopathy in BD, regardless of MR severity. We hypothesise that BD and FED are determined by different genetic mutations and pathophysiological processes, which result in more severe left ventricular remodelling in BD as compared with FED. A better understanding of the genetic and phenotypic differences between BD and FED is crucial to improve patient's risk stratification, diagnostic and therapeutic management. The aim of this project is to prospectively assess the differences in genotype and phenotype between BD versus FED with a focus on left ventricular remodelling, myocardial fibrosis and arrhythmias and its evolution with or without mitral valve surgery. We will recruit 100 patients with FED and BD at 2 large volume centres (Antwerp University Hospital and Maastricht Medical University Center) for genetic analysis and an in-depth phenotyping with 3D-echocardiography and cardiovascular magnetic resonance scan.

Researcher(s)

• Promoter: Van De Heyning Caroline
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Pype Lobke

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Anthracyclines are the mainstay of chemotherapeutic treatment in a wide range of malignancies, including breast cancer. Cardiotoxicity is a well-known and feared adverse effect of anthracyclin therapy and due to the growing population of cancer survivors, cardiovascular disease in these patients is expected to escalate. Unless we can identify high-risk patients for anthracycline therapy, today's breast cancer patients may become tomorrow 's heart failure patients. However, there is an important inte individual susceptibility for the development of cardiotoxicity and at present, it is not possible to predict which patients will develop cardiotoxicity. It was recently shown that genetic variants in titin, an import anchoring protein in the cardiomyocytes, can cause a predisposition to dilated cardiomyopathies and are also more prevalent in chemotherapy-induced cardiotoxicity. In this research project we investigate if mutations in titin increase the susceptibility for cardiotoxicity to anthracyclines, in order to identify high -risk patients. If this can be confirmed, the impact on both the individual patient (morbidity, mortality) and on society will be huge. The development of an hiPSC-CM model harbouring different TTNtv will allow us to test different possible therapeutic and preventive measures for this high risk population.

Researcher(s)

• Promoter: Van Craenenbroeck Emeline
• Co-promoter: Alaerts Maaike

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Sarcopenia, which means loss of muscle mass and function, is an independent predictor of death in heart failure patients with reduced ejection fraction (HFrEF). Traditionally, dynamic resistance training is used to counter muscle loss and is characterized by a concentric phase (=shortening) and an eccentric phase (lengthening) causing movement of the limb. Since muscle strength and muscle mass increase more with eccentric training than conventional concentric training without greater cardiorespiratory demands, this modality seems promising in heart failure patients. In this blinded randomized controlled trial, the effectivity and feasability of eccentric training will be assessed in heart failure patients. Forty patients with HFrEF will be randomly assigned to a Control Group (traditional resistance training + aerobic training) or an Intervention Group (eccentric training + aerobic training). Primary outcome parameters are exercise capacity (VO2 peak), muscle strength and muscle mass. It is hypothesized that greater muscle strength and muscle mass will be obtained in the eccentric training group in comparison with traditional resistance training. This better outcome will influence VO2 peak.

Researcher(s)

• Promoter: Baert Isabel
• Co-promoter: Van Craenenbroeck Emeline

Research team(s)

• Movement Antwerp (MOVANT)

Project type(s)

• Research Project

Abstract

Exercise capacity is markedly depressed in adults with congenital heart disease (ACDH) and associated with an increased risk of hospitalization or death. Right ventricular (RV) function is of major importance in ACHD prognosis. Our group recently demonstrated reduced subclinical RV function in ACHD patients with RV overload. Moreover, in a TOF population, strain measurements could predict functional capacity. In other study populations (HFpEF and PAH patients) coronary microvascular dysfunction (CMD) has been shown to be highly prevalent and associated with worse RV strain and exercise intolerance. To the best of our knowledge, the presence of CMD has not been investigated before in ACHD. We hypothesize that multiple factors including genetics, underlying cardiac abnormality, history of cardiac surgery and RV overload, further aggravated by classical acquired risk factors that are known to induce an inflammatory state and reduce nitric oxide bioavailability promote systemic inflammation leading to endothelial dysfunction. As such we hypothesize that the presence of endothelial dysfunction can act as a prognostic and potential therapeutic marker in ACHD. In this research project, we aim to design a prospective study of CMD in ACHD. Potential correlates of reduced CFR including RV loading conditions, clinical and biochemical markers, systemic endothelial function and echocardiographic data will be investigated as well as the potential therapeutic effect of exercise training.

Researcher(s)

• Promoter: Van Berendoncks An
• Co-promoter: Heidbuchel Hein
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Vanreusel Inne

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Mitral valve prolapse (MVP) is a valvular disorder with a prevalence of 2-3% in the general population. MVP can be associated with mitral regurgitation (MR), congestive heart failure, ventricular arrhythmias and sudden cardiac death. Barlow's Disease (BD) and Fibro-Elastic deficiency (FED) present the 2 most common MVP phenotypes. Recently, several genetic mutations have been identified, however the exact genotype-phenotype correlation remains largely unknown. Furthermore, recent evidence points to the existence of a concomitant cardiomyopathy in BD, regardless of MR severity. We hypothesise that BD and FED are determined by different genetic mutations and pathophysiological processes, resulting in more severe left ventricular (LV) remodelling, more myocardial fibrosis and a higher arrhythmogenic risk in BD as compared with FED. The aim of this project is to prospectively assess the differences in genotype and phenotype between BD and FED with a focus on LV remodelling, myocardial fibrosis and arrhythmias and its evolution with or without mitral valve surgery. We will recruit 170 patients, 110 with FED and 60 with BD, at 2 large volume centres (Antwerp University Hospital and Maastricht Medical University Center) for genetic analysis and an in-depth phenotyping with 3D-echocardiography, cardiovascular magnetic resonance scan and 24h-Holter. Follow-up exams will be performed after 1-year in all included patients.

Researcher(s)

• Promoter: Van De Heyning Caroline
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Pype Lobke

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Cancer survival has increased significantly over the last decades because of improved screening and the development of novel therapies. The downside of this positive evolution is that cancer treatment-related adverse events affecting the quality of life of cancer survivors has become an emerging concern. Physical long-term side effects of anthracycline chemotherapy, such as doxorubicin (DOX) and Cisplatin (CIS), include cardiovascular complications (heart failure), peripheral fatigue and muscle mass loss (wasting). While the cardiovascular toxicity of DOX has been extensively studied, this project aim to investigate the effects of DOX and/or CIS on skeletal muscle structure and (mitochondrial) metabolism. Additionally, we will evaluate the possible beneficial effect of physical exercise as a strategy to protect against DOX and CIS induced myotoxicity. This project aims to lay the foundation of a novel joint research line of the research groups of Movant, Cardiovascular Disease and Physiopharmacology to exploit scientific and operational synergies.

Researcher(s)

• Promoter: van Breda Eric
• Co-promoter: Guns Pieter-Jan
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Van Asbroeck Birgit

Research team(s)

• Movement Antwerp (MOVANT)

Project type(s)

• Research Project

Abstract

Anthracyclines are the mainstay of chemotherapeutic treatment in a wide range of malignancies, including breast cancer and frequent childhood cancers. Due to a growing population of cancer-survivors, the importance of long-term complications of anti-cancer treatment has increased. Today's breast cancer patients may become tomorrow's heart failure patients. There is an important inter individual susceptibility for the development of cardiotoxicity. This variation is not fully explained by differences in clinical risk factors. Therefore, it is suggested that genetic variations may play a role. It was recently shown that genetic variants in titin, an import anchoring protein in the cardiomyocytes, can cause a predisposition to dilated cardiomyopathies that are clinically similar to chemotherapy-induced cardiotoxicity In this research project we aim to investigate whether mutations in important structural cardiac genes, more specific titin, can cause an increased susceptibility for cardiotoxicity.

Researcher(s)

• Promoter: Van Craenenbroeck Emeline

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

New drug candidates often have off-target effects resulting in adverse events, thus representing a major limitation for drug R&D. Safety Pharmacology (SP) aims to detect, understand and reduce undesirable pharmacodynamic effects early-on. Especially, cardiovascular (CV) toxicity is problematic, as it is the most prevalent reason for failure during preclinical development. Moreover, CV toxicity remains a key reason for drug attrition during clinical development and beyond. This indicates current SP screens fail to detect a number of (late-onset) functional or structural CV toxicities. Additionally, SP uses a significant number of laboratory animals, thereby creating opportunities for a better implementation of the 3Rs. The vision of INSPIRE is to advance and "inspire" SP by exploring new technological capabilities (WP1), addressing emerging CV concerns (WP2) and delivering new validated solutions for CV safety screening (WP3). To this end, INSPIRE unites expertise from academic teams, technology-providers, pharmaceutical companies, regulators and hospitals to create a European training platform for 15 Early Stage Researchers (ESRs). Key innovative aspects of INSPIRE include: i) in vitro humanized cardiomyocytes assays, ii) unparalleled in vivo hardware/software solutions, iii) in silico predictions of haemodynamics, iv) mass spectroscopy imaging of drug exposure, v) exploration of mechanisms of late-onset CV toxicity, as observed in cardio-oncology, and vi) early integration of feedback from industry and regulators. Overall, INSPIRE constitutes a multidisciplinary and intersectoral training programme (WP4) with a balanced combination of hands-on research training, intersectoral secondments, local courses and network-wide events on scientific and transferable skills, enabling future R&I collaborations. Hence, INSPIRE will equip the future generation of SP scientists with a wide range of scientific knowledge and the ability to adapt to a dynamic ever-changing industry.

Researcher(s)

• Promoter: Guns Pieter-Jan
• Co-promoter: De Meyer Guido
• Co-promoter: Heidbuchel Hein
• Co-promoter: Martinet Wim
• Co-promoter: Segers Vincent
• Co-promoter: Van Craenenbroeck Emeline

Research team(s)

• Physiopharmacology (PHYSPHAR)

Project type(s)

• Research Project

Abstract

Anthracyclines are the mainstay of chemotherapeutic treatment in a wide range of malignancies, including breast cancer and frequent childhood cancers. Due to a growing population of cancer-survivors, the importance of long-term complications of anti-cancer treatment has increased. Today's breast cancer patients may become tomorrow's heart failure patients. There is an important inter individual susceptibility for the development of cardiotoxicity. This variation is not fully explained by differences in clinical risk factors. Therefore, it is suggested that genetic variations may play a role. It was recently shown that genetic variants in titin, an import anchoring protein in the cardiomyocytes, can cause a predisposition to dilated cardiomyopathies that are clinically similar to chemotherapy-induced cardiotoxicity In this research project we aim to investigate whether mutations in important structural cardiac genes, more specific titin, can cause an increased susceptibility for cardiotoxicity.

Researcher(s)

• Promoter: Van Craenenbroeck Emeline
• Co-promoter: Heidbuchel Hein
• Co-promoter: Loeys Bart
• Fellow: Boen Hanne

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

The burden of heart failure is substantial and likely to grow, urging for development of new therapies. Exercise training is one of the most successful therapies for heart failure but unfortunately, 20% of patients show no response and thus fail to improve prognosis. MicroRNA were recently put forward as key players in the response to exercise training. Identification of exercise-related microRNA could lead towards novel microRNA-based therapies that mimic exercise effects and could lead to a microRNA biomarker panel that can assist in tailoring of training programmes. Preliminary data from our group support this hypothesis: by performing a large unbiased screening, we designed a microRNA fingerprint that discriminates responders from non-responders to exercise training. We anticipate that the microRNA fingerprint may guide us towards microRNA that are crucial in a favorable adaptation to exercise. This translational project proposal involves both fundamental research (an animal study on microRNA-based therapy, including in vitro studies to gain mechanistic insight in microRNA-mRNA targets) and clinical translation (a prospective clinical trial to assess the predictive capacity of circulating microRNA for tailoring exercise therapy). This bedside-to-bench-and-back approach will maximize the potential for translation in relevant clinical results. In conclusion, we will use exercise as a model to discover candidate microRNA for therapy and to guide patient-tailored therapy.

Researcher(s)

• Promoter: Heidbuchel Hein
• Fellow: Van Craenenbroeck Emeline

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

MicroRNAs are negative regulators of gene expression by inhibition of mRNA translation in the cell cytoplasm. MicroRNAs can be released into the circulation upon cell injury or as part of intercellular communication. Together with their remarkable stability in plasma, this feature makes microRNAs attractive as biomarkers. Physical exercise may alter gene expression through an effect on circulating microRNA. Exercise training is one of the most efficacious ways to improve physical performance, quality of life and to reduce morbidity and mortality in patients with heart failure. However, recent insights show that exercise-induced maladaptations may also lead to pathology, for example exercise-induced arrhythmogenic right ventricular cardiomyopathy, a condition well known in athletes. In this project, we will focus on the role of microRNA in cardiovascular adaptation to exercise at both spectra: the beneficial effects of exercise in heart failure with reduced ejection fraction (HFrEF) as well as exercise-induced arrhythmogenic right ventricular cardiomyopathy (EI-ARVC) in athletes. MicroRNA's could serve as marker of and may even play a mechanistic role in the respons to exercise during cardiac rehabilitation. In El-ARVC, they could serve as diagnostic markers for this disease. In both conditions, microRNA's may offer insights into the underlying mechanisms that are involved in exercise-induced remodeling under the physiological stress of exercise.

Researcher(s)

• Promoter: Heidbuchel Hein
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Witvrouwen Isabel

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Heart failure is the cardiovascular epidemic of the 21st century, due to population ageing and improved cardiovascular therapy. Half of heart failure patients has a preserved ejection fraction, but little is known about these 'HFpEF' patients. HFpEF pathophysiology is incompletely understood, and no existing treatment is able to improve prognosis (50% mortality at 5 years). A complicating factor is the heterogeneity of HFpEF patients: different phenotypes seem to exist, but in large clinical trials these are all classified under one 'HFpEF' category. MicroRNA seem to play an important role in HFpEF pathophysiology. MicroRNA are epigenetic regulators controlling countless biological processes and are stable in the circulation, which makes them attractive biomarkers. Also, microRNA-based therapy is easy to administer and expected effects are large, due to numerous downstream targets. We recently discovered that microRNA-181c is linked to the response to exercise training in HFpEF patients. Additionally, we found increased microRNA-181c in hearts of an ageing mouse model of HFpEF. In this project, we want to establish the diagnostic and therapeutic potential of microRNA-181c in HFpEF. Our translational approach guarantees relevant results: on one hand, we use several animal models of HFpEF (representing different clinical phenotypes) to test microRNA-181c in a therapeutic setting, on the other hand we set up a longitudinal clinical study to check the diagnostic potential of microRNA-181c with regards to the different HFpEF phenotypes. This study will evaluate microRNA-181c as a possible biomarker and therapeutic target in HFpEF. The translational design will facilitate future clinical trials. Finally, this project will gather much-needed insight in the pathophysiology of HFpEF.

Researcher(s)

• Promoter: Van Craenenbroeck Emeline
• Fellow: Boen Jente

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Cardiovascular disease is the leading cause of death in Europe and is strongly related to a sedentary lifestyle. In parallel with a modern inactivity pandemic, the past 2 decades have witnessed an increase in the number of middle-aged and older individuals engaging incompetitive endurance sports events. This increasing popularity of endurance sports implies that a greater proportion of individuals participating in high-intensity sport has a higher cardiovascular risk profile. Coronary artery disease is by far the most common cause of sudden cardiac death in senior athletes. Cases of sudden cardiac death are often widely publicized in the media, and are accompanied by questions on its relation with the sports activity and how it could have been prevented. Retrospective observations provide some reassurance, but have been difficult to interpret given major differences between athletic and referent populations in cardiovascular risk factors such as smoking and socio-economic status. Concerns regarding a potential 'overdose' of exercise are further nourished by data in the literature that have linked long-term endurance exercise with an excess of arrhythmias. The aim of this project is to discern both preventive and adverse effects of long-term endurance exercise. By comparing a group of lifelong endurance athletes, engaged in endurance sports since the age of 25 years, a group of late-onset older endurance athletes, performing endurance exercise since only 6 to 36 months, and a sedentary cohort we will specifically assess the benefits and risks related to the age of onset of endurance exercise. As primary endpoint we will assess the prevalence of coronary atherosclerosis using coronary artery calcium scoring. We will evaluate if a possible beneficial effect of lifelong endurance exercise on coronary artery disease is associated with an increased risk of adverse effects, such as an increased incidence of atrial fibrillation or significant myocardial fibrosis.

Researcher(s)

• Promoter: Heidbuchel Hein
• Co-promoter: Van Craenenbroeck Emeline

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

MicroRNAs are negative regulators of gene expression by inhibition of mRNA translation in the cell cytoplasm. MicroRNAs can be released into the circulation upon cell injury or as part of intercellular communication. Together with their remarkable stability in plasma, this feature makes microRNAs attractive as biomarkers. Physical exercise may alter gene expression through an effect on circulating microRNA. Exercise training is one of the most efficacious ways to improve physical performance, quality of life and to reduce morbidity and mortality in patients with heart failure. However, recent insights show that exercise-induced maladaptations may also lead to pathology, for example exercise-induced arrhythmogenic right ventricular cardiomyopathy, a condition well known in athletes. In this project, we will focus on the role of microRNA in cardiovascular adaptation to exercise at both spectra: the beneficial effects of exercise in heart failure with reduced ejection fraction (HFrEF) as well as exercise-induced arrhythmogenic right ventricular cardiomyopathy (EI-ARVC) in athletes. MicroRNA's could serve as marker of and may even play a mechanistic role in the respons to exercise during cardiac rehabilitation. In El-ARVC, they could serve as diagnostic markers for this disease. In both conditions, microRNA's may offer insights into the underlying mechanisms that are involved in exercise-induced remodeling under the physiological stress of exercise.

Researcher(s)

• Promoter: Heidbuchel Hein
• Co-promoter: Van Craenenbroeck Emeline
• Fellow: Witvrouwen Isabel

Research team(s)

• Cardiovascular diseases (CARDIOVASC)

Project type(s)

• Research Project

Abstract

Diseases of the heart and blood vessels are the world's leading killers. Patients that have suffered from these diseases are advised to engage in a rehabilitation program, with the aim to prevent recurrence or deterioration of the disease. Unfortunately, despite the proven benefit, patients often do not adhere to this program. It is thus important to implement new strategies with the goal to sustain a healthy lifestyle in subjects with heart disease after being hospitalised. The hypothesis is that telerehabilitation can help to reach this goal. Telerehabilitation means that a patient is coached through his rehabilitation program from a distance. Several devices, most of them wearable, are used to monitor various parameters (physical activity, heart rate, weight...) and this information is sent to the doctor by Internet or telephone network. This project will investigate the effectiveness of a telerehabilitation program on the important risk factors for diseases of the heart and blood vessels on the physical fitness of the patient and on the recurrences and deteriorations of the diseases by means of the telerehabilitation trial. In this trial patients with different types of heart disease will be monitored during a long follow-up period. Additionally a Cardiac Patient Training Companion will be designed and developed. This is a tool that will assist the patient in his telerehabilitation program. The Companion will monitor, coach and educate the patient about his condition.

Researcher(s)

• Promoter: Van Craenenbroeck Emeline
• Fellow: Frederix Ines

Research team(s)

Project type(s)

• Research Project

Abstract

Heart failure is the cardiovascular epidemic of the 21st century and despite improved medical management, prognosis remains grim. Exercise training is a powerful therapeutic strategy to improve morbidity and mortality in heart failure. However, the individual response to exercise training is highly variable among patients. Research into the phenomenon of high responders and low responders may provide helpful insights into the beneficial effects of exercise training. In this regards, the emerging field of exercise epigenomics is extremely promising. The potential of microRNA to become unique, blood-based epigenetic biomarkers for cardiovascular health and aerobic capacity is high. As such, they can assist in a tailored approach that offers safer and more effective therapy and avoids unnecessary treatments. In addition, an in-depth study of miRNA regulation in 'low-responders' versus 'high-responders', opens entirely new therapeutic avenues, either through a drugable antagomiRs, or trough identification of new therapeutic targets.

Researcher(s)

• Promoter: Van Craenenbroeck Emeline
• Fellow: Van Medegael Laure
• Fellow: Witvrouwen Isabel

Research team(s)

Project type(s)

• Research Project

Abstract

The present project has three main aims. The first is to determine the role of endothelial dysfunction in exercise intolerance of CHF patients and to study the effect exercise training. Secondly, we will further explore the potential role of microRNAs in endothelial dysfunction. These microRNAs are short circulating molecules that regulate gene expression. We will investigate if such microRNAs might be useful as biomarkers for exercise capacity in CHF patients. The third aim is to investigate and possibly modify crucial pathways that are responsible for the bone marrow dysfunction that is found in CHF patients. This bone marrow malfunction also affects the bone marrow derived progenitor cells that are crucial in the process of endothelial repair.

Researcher(s)

• Promoter: Vrints Christiaan
• Fellow: Van Craenenbroeck Emeline

Research team(s)

Project type(s)

• Research Project

Abstract

This project represents a research contract awarded by the University of Antwerp. The supervisor provides the Antwerp University research mentioned in the title of the project under the conditions stipulated by the university.

Researcher(s)

• Promoter: Van Craenenbroeck Emeline

Research team(s)

Project type(s)

• Research Project

Abstract

This project represents a research contract awarded by the University of Antwerp. The supervisor provides the Antwerp University research mentioned in the title of the project under the conditions stipulated by the university.

Researcher(s)

• Promoter: Conraads Viviane
• Promoter: Vrints Christiaan
• Co-promoter: Van Craenenbroeck Emeline
• Co-promoter: Vrints Christiaan
• Fellow: Nollet Evelien

Research team(s)

Project type(s)

• Research Project

Abstract

The proposed project approach will create unique opportunities to describe the extent of bone marrow dysfunction in patients with ischemic heart disease and to explore underlying mechanisms. As such, it might be possible to identify reversible pathways that should be targeted in order to functionally rejuvenate "sick" autologous bone marrow-derived stem cells. The combination of gene and cell therapy has the potential to create tailored therapy, ultimately improving morbidity and mortality of patients with cardiovascular disease.

Researcher(s)

• Promoter: Conraads Viviane
• Promoter: Vrints Christiaan
• Co-promoter: Cools Nathalie
• Co-promoter: Hoymans Vicky
• Co-promoter: Rodrigus Inez
• Co-promoter: Van Craenenbroeck Emeline
• Co-promoter: Vrints Christiaan

Research team(s)

Project type(s)

• Research Project

Abstract

This project represents a research contract awarded by the University of Antwerp. The supervisor provides the Antwerp University research mentioned in the title of the project under the conditions stipulated by the university.

Researcher(s)

• Promoter: Van Craenenbroeck Emeline

Research team(s)

Project type(s)

• Research Project

Abstract

In this study, the effect of exercise on the number and function of circulating endothelial progenitor cells (EPC), is evaluated in chronic heart failure patients. A single bout of maximal exercise as well as a physical training program are investigated as stimuli for the release of EPC. Underlying physiological mechanisms are assessed and special attention goes to homing factors, nitric oxide and oxidative stress. Healthy subjects and patients with coronary artery disease will serve as a control group.

Researcher(s)

• Promoter: Conraads Viviane
• Co-promoter: Vrints Christiaan
• Fellow: Van Craenenbroeck Emeline

Research team(s)

Project type(s)

• Research Project

Abstract

In this study, the effect of exercise on the number and function of circulating endothelial progenitor cells (EPC), is evaluated in chronic heart failure patients. A single bout of maximal exercise as well as a physical training program are investigated as stimuli for the release of EPC. Underlying physiological mechanisms are assessed and special attention goes to homing factors, nitric oxide and oxidative stress. Healthy subjects and patients with coronary artery disease will serve as a control group.

Researcher(s)

• Promoter: Vrints Christiaan
• Co-promoter: Conraads Viviane
• Co-promoter: Van Bockstaele Dirk
• Fellow: Van Craenenbroeck Emeline

Research team(s)

Project type(s)

• Research Project