Research Tom Vanden Berghe

Abstract

The Cell Death lab studies the molecular stress responses which affect cell plasticity (autophagy), cell death (apoptosis, necroptosis, ferroptosis, pyroptosis & netosis), or senescence. This research cluster investigates these mechanisms to improve diagnostic tools or intervention strategies in cell death- or inflammation-driven disease areas. We perform bench-to-bed-oriented research covering biochemistry, cell-based assays, preclinical rodent experimental models as well as validation in patient samples using cutting-edge technologies & integrative -omics approaches.

Researcher(s)

• Promoter: Vanden Berghe Tom

Research team(s)

Project type(s)

• Research Project

Abstract

Ferroptosis is an iron-catalyzed form of regulated cell death that occurs due to excessive lipid peroxidation in cellular membranes. Since the discovery in 2012, the high clinical relevance of ferroptosis in e.g. diseases driven by ischemia reperfusion injury (IRI) has boosted the development of ferroptosis therapeutics. To date, the most potent inhibitors in vitro are lipophilic radical trapping antioxidants (RTAs). Our-in house developed and patented candidate lead RTA (UAMC-3203), proved to be superior to the benchmark inhibitors in protecting against organ injury and is therefore considered an excellent drug candidate for clinical translation. At present, the success of transplantation is hampered by the adverse effect of IRI. Supported by multiple preclinical studies, ferroptosis targeting appears a promising strategy to block IRI. We are currently exploring the implementation of ferroptosis inhibitor strategies in the clinical practice of transplantation. Since the in vivo efficacy of UAMC-3203 to block ferroptosis or IRI in the lung is still unclear, we want to monitor ferroptosis during lung IRI in mouse, pig and human and determine its therapeutic potential using UAMC-3203 to block lung IRI in mice and pig.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Fellow: Veeckmans Geraldine

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Neuroblastoma is the most common solid tumor outside the brain of infants and very young children. A substantial part of neuroblastoma patients presents with high-risk neuroblastoma disease. In fact, these children have a poor prognosis, do not respond to therapy or even relapse. Therefore, there is an urgent need to find novel treatment strategies. Recently, the Vanden Berghe lab discovered a new approach to kill aggressive therapy resistant neuroblastoma cells in mice by inducing ferroptotic cell death in cancer cells. Epigenetic changes have been reported as one of the mechanisms for anti-tumor drug resistance. The aim of this project is to understand how the epigenetic modifications affect ferroptosis susceptibility/resistance in neuroblastoma and how reverting these changes could recondition cells to ferroptotic cell death.

Researcher(s)

• Promoter: Vanden Berghe Tom

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

The complexity of critical illness in intensive care essentially requires a precision approach. Organ failure and sepsis are key detrimental factors in critical illness, and fundamentally driven by an auto-amplifying loop of cell death and inflammation. This process feeds dynamic disease fluctuations and heterogeneity in critical care, which might partially explain inconsistent translatability. Patients with similar clinical presentations typically have different cellular and molecular responses due to individual differences and co- morbidities. To deal with this form of heterogeneity, innovative biomarkers with predictive value are needed to allow determining subtypes of clinically similar patients. There is a growing list of circulating detrimental biomolecules related to some forms of regulated non-apopoptic cell death (i.e. so-called ferroptotic and pyroptotic cell death), which are druggable and allow stratifying critically ill patients. Actually, we discovered that therapeutic targeting ferroptosis or pyroptosis respectively increased survival in experimental models of multi organ failure or septic shock. To allow follow-up of clinical intervention studies, real-time diagnostics for these detrimental factors are needed. Dynamic monitoring of a panel of cytokines in critically ill patients showed prognostic value for 30-day survival, septic shock and organ injury. To level up our proof of concept, we want to conduct a translational study in critically ill patients by using real-time immunodiagnostics to detect ferroptosis and pyroptosis; which should allow quick stratification for the linked targeted therapies thereby preventing organ/systemic dysfunction and mortality. To detect general tissue injury due to excess cell death, we also optimized a procedure to episequence plasma cell free DNA (cfDNA) using real-time Oxford Nanopore Technology. As a potential future complementary diagnostic tool, we want to determine the diagnostic power of nanopore episequencing to detect tissue specific cell death. To process the clinical and molecular fingerprint of the critically ill determined in biofluids, we additionally use big data mining approaches in these phenotypically well-characterized patients. Precision intervention based on innovative real-time molecular diagnostics and stratification could bring diagnostics in intensive care into the 21st century and pinpoint which patients are likely to benefit from a certain treatment.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Co-promoter: Jorens Philippe
• Co-promoter: Koljenovic Senada

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Epigenetic regulation has been shown to be involved in ferroptosis therapy resistance. Ferroptosis is increasingly recognized as a promising treatment option for cancer therapy, while diagnostic tools that predict tumor's sensitivity for ferroptosis are not yet developed. Therefore, in this industrial PhD project (Baekeland), a multi-step approach will be applied to (i) identify a "ferroptomics" epifingerprint that determine this ferroptosis sensitivity, (ii) develop a sensitive, cost-effective and portable nFERROCATCH assay to predict ferroptosis sensitivity based on TGS, one of the strongholds of OHMX.bio (precision diagnostics based on Nanopore sequencing) and (iii) validate the assay using experimental and clinical samples. This nFERROCATCH assay will be offered as a fee for service and can also be further commercialized.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Co-promoter: Vanden Berghe Wim
• Fellow: Vintea Iuliana

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Every day, billions of cells in the human body undergo cell death. This process ensures tissue homeostasis and elimination of harmful cells. Moreover, cell death is induced in response to microbial insults as a way to eliminate the infected cells and to alert the immune system through the release of danger signals. Accordingly, unwanted and excessive cell death exacerbate immune responses, and is therefore suspected to be at the origin of various human inflammatory pathologies. Cell demise can occur in different ways, providing each form of cell death with a specific flavor. However, the mechanisms that regulate the induction and execution of these different cell death modalities, their respective and combined contribution to anti-microbial immunity or their precise detrimental consequences in inflammatory diseases remain unclear. This absence of fundamental knowledge limits the possibilities of therapeutic intervention. The proposed CD-INFLADIS research program aims at providing answers to these questions by setting up a strong quadruple interaction combining basic cell biology studies, medicinal chemistry, experimental mouse models of diseases and analysis of human clinical samples. As infectious and inflammatory diseases represent an increasing burden for the human health, we expect the major findings of our consortium to have important societal impact.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Co-promoter: Augustyns Koen

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Neuroblastoma is the most common solid tumor outside the brain of infants and very young children. A substantial part of neuroblastoma patients presents with high-risk neuroblastoma disease. In fact, these children have a poor prognosis, do not respond to therapy or even relapse. Therefore, there is an urgent need to find novel treatment strategies. Recently, our research group discovered a new approach to kill aggressive therapy-resistant neuroblastoma cells in mice by inducing a sort of biological rusting in cancer cells, called ferroptosis. Ferroptosis is a type of cell death that rusts away the cellular membrane, which quickly kills the cells. By using nanoparticles, the lab was able to minimize side effects of treatment and enhance tumor targeting. However, to get full tumor regression without relapse using a nanomedicinal approach, it is needed to further improve the efficacy of targeting ferroptosis in neuroblastoma. The aim of this project is to recondition high-risk neuroblastoma to a ferroptosis sensitive state, by acting on anti-ferroptosis mechanisms in cancer cells. In addition, ferroptosis-sensitizing compounds will be encapsulated in lipid nanoparticles, currently used for the Covid-19 RNA vaccines. These ferroptosis-sensitizing nanomedicines will be tested and validated in cell- and patient-derived high-risk neuroblastoma mouse models and provide a steppingstone to clinical investigation of ferroptosis targeting as anti-cancer therapy.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Co-promoter: Hassannia Behrouz
• Fellow: Koeken Ine

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Arterial media calcification (AMC) is the deposition of calcium-phosphate crystals in the medial layer of the arterial wall and is an independent risk factor for cardiovascular morbidity/mortality. Efficient treatment for this lethal, highly prevalent pathology is lacking. Vascular smooth muscle cells, the key cell type in AMC, under oxidative stress transdifferentiate into cells with bone-forming capacity or die. It is not clear, however, which cell death type is most important. Ferroptosis, a recently discovered regulated type of cell death, is the result of iron-catalyzed, oxidative stress-induced membranous lipid peroxidation. Several arguments from literature and preliminary results from our lab put forward a role for iron accumulation, lipid peroxidation/ferroptosis in the process of AMC. This project aims to further substantiate this role by (i) exploring the AMC-aggravating effect of iron and (ii) the genetic induction of vascular smooth muscle cell-lipid peroxidation, in order to put forward lipid peroxidation as a novel target to treat AMC. Lipid peroxidation can be prevented by membranous radical trapping. Since potent membranous radical traps were developed in-house, we will have the unique opportunity to test these patented molecules for their ability to halt AMC. AMC-therapy development often stumbled over osseous side-effects (crystal deposition was inhibited in bone next to vessels). Membranous radical trapping therapy should overcome this problem.

Researcher(s)

• Promoter: Verhulst Anja
• Co-promoter: Vanden Berghe Tom
• Fellow: Van den Branden Astrid

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

The success of transplantation is hampered by a shortage in suitable organ grafts and the adverse effects of ischemia reperfusion injury (IRI). Inflammation and cell death in the transplanted organ, caused by the activation of the innate immune system as part of the IRI process, leads to primary graft dysfunction (PGD). Transplant recipients that suffer from severe PGD have an increased risk for early and late morbidity and mortality. The organ perfusion strategy was developed to increase the number of available grafts. During the ex situ phase between organ retrieval and transplantation, machine perfusion offers a unique window of opportunity for organ graft modulation to target IRI due to ferroptosis. Ferroptosis is an iron-dependent type of cell death in which oxidative stress initiates excessive lipid peroxidation of cellular membranes leading to cell death. Our in-house developed and patented third generation ferroptosis inhibitors show superior protection in preclinical models of organ injury and are therefore good drug candidates to block injury during transplantation. In this project, we will firstly verify the efficacy of the lead ferroptosis inhibitor in protecting against ferroptosis using genetic organ injury models along experimental IRI or transplantation models in rodents. We will focus on liver, kidney and lungs as vital organs. Secondly, we will analyse the efficacy of adding our lead ferroptosis inhibitor to perfusate during normothermic machine perfusion preceding ex situ reperfusion in pigs. In parallel, we will evaluate the potential of ferroptosis inhibitors to recondition human organ grafts. This research plan is a first step to implement ferroptosis inhibitory strategies in the clinical practice of transplantation, which is a steppingstone for building a spin-off case in ferroptosis therapeutics.

Researcher(s)

• Promoter: Vanden Berghe Tom

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the liver component of the metabolic syndrome and reaches global epidemic proportions. Isolated steatosis is the most common form, but some patients progress towards nonalcoholic steatohepatitis (NASH). The latter predisposes to fibrosis, cirrhosis and cardiovascular disease. Determinants of progression towards NASH are unclear. In isolated steatosis, we have previously shown the presence of increased hepatic vascular resistance which potentially leads to low-flow ischemia and hepatic parenchymal hypoxia, triggering the transition to steatohepatitis. We hypothesize that this chronic hepatic hypoxia induces a specific subtype of cell death in steatotic hepatocytes, i.e. ferroptosis. This recently described cell death is mediated by iron-catalyzed membrane lipid peroxides and has been suggested to play an important role in NAFLD. We will study the presence of hepatic ferroptosis in relation to disease severity in a large human NAFLD cohort. The potential of hypoxia to induce ferroptosis will be assessed in an in vitro NAFLD model to study the trigger of ferroptosis. Furthermore, we will objectify the presence of hepatic parenchymal hypoxia and ferroptosis in a murine dietary model of NAFLD. Afterwards, we will test the potential of vasodilatory compounds (which reduce hepatic hypoxia) and a novel third-generation ferroptosis inhibitor to inhibit progression towards NASH and treat an established NASH in the murine dietary model.

Researcher(s)

• Promoter: Francque Sven
• Co-promoter: Vanden Berghe Tom
• Co-promoter: Van Eyck Annelies
• Fellow: Peleman Cédric

Research team(s)

• Laboratory Experimental Medicine and Pediatrics (LEMP)

Project type(s)

• Research Project

Abstract

The Research Consortium of Excellence Infla-Med combines multidisciplinary expertise of eight research groups from two faculties to perform fundamental and translational research on inflammation, including: inflammatory gastrointestinal, cardiovascular, lung and kidney disorders, sepsis and allergies, as well as parasitic diseases, thereby focusing on specific inflammatory cell populations, including monocytes/macrophages, mast cells, basophils and lymphocytes. The approach of the Infla-Med consortium is twofold. Firstly, fundamental studies are performed to unravel the pathophysiological mechanisms underlying inflammatory conditions in order to enable more rational, targeted and effective intervention strategies. Secondly, Infla-Med aims to identify and validate novel therapeutic targets by screening chemical compounds in early drug discovery studies and by using an extensive platform of in vitro assays and in vivo models. The close collaboration with the Antwerp University Hospital (UZA) creates the opportunity to directly translate and clinically validate experimental findings. Thereby, Infla-Med contributes to two Frontline Research Domains of the University of Antwerp: 'Drug Discovery and Development' and 'Infectious Diseases'. Over the past four years, the multidisciplinary collaborations within Infla-Med have proven to be very successful and productive. By integrating the Infla-Med unique expertise on drug development, in vitro assays and clinically relevant animal models (validated with human samples), significant competitive funding has been acquired at European, national and UAntwerp levels with a success rate of more than 45%, which is far above the (inter)national average. Noteworthy, several Infla-Med projects have also made the transition towards valorization, demonstrating that Infla-Med results obtained from both fundamental research and well-designed preclinical studies can successfully be translated into clinical trials.

Researcher(s)

• Promoter: De Meyer Guido
• Co-promoter: Augustyns Koen
• Co-promoter: Caljon Guy
• Co-promoter: De Meester Ingrid
• Co-promoter: De Winter Benedicte
• Co-promoter: Ebo Didier
• Co-promoter: Heidbuchel Hein
• Co-promoter: Vanden Berghe Tom

Research team(s)

• Physiopharmacology (PHYSPHAR)

Project website

Project type(s)

• Research Project

Abstract

This multi-centre, practice-oriented, repurposing, double-blind, placebo-controlled, randomized clinical trial evaluates the effect of metformin treatment on the progression of chronic renal failure

Researcher(s)

• Promoter: D'Haese Patrick
• Promoter: Vanden Berghe Tom
• Co-promoter: De Broe Marc
• Co-promoter: D'Haese Patrick

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Disorders of mineral metabolism, specifically calcium and phosphorus homeostasis, are common in patients with chronic kidney disease (CKD), diabetes and osteoporosis. CKD is a world-wide recognized public health problem affecting 8-16% of the world population. Also the prevalence of diabetes and osteoporosis is high (12.3% for diabetes and 30% for osteoporosis of all postmenopausal women) and still increasing. Essentially, these three disorders of mineral metabolism typically share interconnected features including renal failure, vascular calcification and aberrant bone metabolism. CKD represents a progressive loss of renal function over a period of months or years ultimately leading to end-stage renal disease, which inevitably requires renal replacement therapy, i.e. dialysis and kidney transplantation. Vascular calcification in the medial layer of blood vessels is a major clinical problem and the most important cause of death in CKD patients. Structures similar to bone and cartilage are detected in the calcified arterial wall thereby mimicking bone formation. In addition, the disturbed mineral metabolism in CKD patients leads to the development of renal osteodystrophy which ultimately result in a reduced bone strength and increased incidence of bone fractures. The concomitant occurrence of a disturbed bone metabolism with a pathological calcification of the vessel wall in CDK patients is referred to as "the calcification paradox", which is also observed in diabetes and osteoporosis patients. The strong increase in the number of elderly boosts the prevalence of aging-related disorders such as CKD, diabetes and osteoporosis, and herewith the interest of pharmaceutical companies in clinical as well as preclinical research on these disorders. During the last decade, the Laboratory of Pathophysiology has developed unique animal models for the in vivo investigatation of different aspects of this interconnected triad (kidney, vessels and bone) in mineral metabolism disorders. These animal models besides investigation of fundamental mechanisms underlying these pathophysiological processes also allow to intervene in these processes by candidate therapeutics. This unique combination of animal models, substantiated by fundamental pathological knowledge, resulted in a cutting edge platform for preclinical (animal model) drug testing, which successfully attracted contract research with industrial partners resulting in an income of 500k€/year during the last decade. From our unique position at the interface between academics and industry, we note that industrial interest is shifting from symptomatic treatment (hypertension or hyperphosphatemia) towards a direct interference with CKD and vessel wall calcification. To anticipate this trend and level-up the valorization potential of our current platform of animal models, this IOF-service platforms project aims to expands its portfolio and setup novel innovative animal models to guarantee a further increase in industrial revenue.

Researcher(s)

• Promoter: Verhulst Anja
• Co-promoter: Vanden Berghe Tom
• Co-promoter: Vervaet Benjamin

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Ferroptosis is an iron-catalyzed form of regulated necrosis, which is shown to be detrimentally involved in several experimental disease models, such as acute kidney/liver injury and neurodegeneration. Glutathione peroxidase 4 (GPX4) is the central enzyme protecting the cell from excessive lipid peroxidation, which is the key execution process in ferroptosis. A high-throughput screening performed by the Stockwell Lab (Columbia University, US) led to the discovery of ferrostatin-1 (Fer1) as a potent in vitro inhibitor of ferroptosis. In vivo however, the molecule suffers from instability. Therefore, we developed ferrostatin-analogues with improved efficacy, solubility and stability. Ongoing research, in the framework of an FWO research project and an FWO-EOS project, illustrates that our patented lead Fer1--analogue UAMC-3203 is superior as compared to the benchmarks in several ferroptosis-driven experimental disease mouse models. The aim of this project is to study aspects of absorption, distribution, metabolism and excretion of the potential lead ferroptosis inhibitor UAMC-3203 in mice and rats. The results of this POC project should deliver an extended ADME-profile, verify its ability to cross the blood-brain-barrier and validate the possibility to administer UAMC-3203 orally. This will increase the valorisation potential of this compound. As the number of potential applications is relatively big, building a spin-off case for evaluation by seasoned investors and business professionals is likely the most suitable valorisation strategy.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Co-promoter: Augustyns Koen
• Co-promoter: van Nuijs Alexander

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Neuroblastoma (NB) is the most common solid tumor outside the brain of infants and very young children. The aggressive forms of neuroblastoma are often accompanied by an increased resistance to current chemotherapies due to defects in the molecular mechanisms that normally leads to the death of cancer cells. Therefore, the challenge is to find new molecular mechanisms to kill the cancer cells. Recently, we discovered a new approach to kill aggressive therapy-resistant neuroblastoma in mice by triggering a sort of biological rusting in cancer cells called ferroptosis. Ferroptosis is an iron-driven oxidation reaction of the membranes of cancer cells, which quickly kills the cells. By using nanoparticles, we were able to minimize the side effects of treatment and enhanced tumor targeting. However, to get tumor regression without relapse using a nanomedicinal approach, it is needed to further improve and validate the efficacy of ferroptosis targeting in neuroblastoma. In this project, we will use different genetic and pharmacological approaches to improve the therapeutic applicability of ferroptosis in neuroblastoma. To this end, we will use genomically well-characterized patientderived neuroblastoma models to identify potent ferroptosis triggers in order to achieve more effective suppression of tumor growth and avoid relapses.

Researcher(s)

• Promoter: Vanden Berghe Tom

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

We request funding for two basic infrastructure equipment to measure cell death along any other biochemical parameter that is crucial to determine the mode of cell death such as caspase activation, reactive oxygen species, calcium, mitochondrial membrane potential, lysosomal leakage and lipid peroxidation: 1) FLUOstar® Omega plate reader with atmospheric control unit and 2) BD Accuri C6 Plus personal flow cytometer. These two instruments are perfectly complementary, while the Fluostar provides average values measured on cell populations seeded in any plate up to 384-well plates, the Accuri analyzes at the single cell level allowing to detect heterogenous responses. If the transition from Pathophysiology lab (headed by Patrick D'Haese until 2020) to Cell Death and Inflammation research lab (headed by Tom Vanden Berghe from 2020 onwards) is to proceed smoothly, the investment in this basic but crucial equipment to analyze cell death and related biochemical features is highly needed. Investment in the cell death platform at UAntwerp will boost the recently initiated collaborations in the field of cell death research at UAntwerp. Cell death research is highly present but scattered within the Faculties of FBD and GGW, therefore we initiated monthly sessions of the Cell Death Hot Talks (supported by the OEC Infla-Med). These sessions will (i) increase the exchange on ongoing cell death research, (ii) lead to sharing tools and (iii) boost potential collaborations. Along this line of sharing cell death related expertise and tools, there is a high need to setup a platform to measure and type the mode of cell death within the faculties of FBD and GGW. This investment fits well in the long-term strategic plan in which cell death is one of the four research clusters within the Department of Biomedical Sciences. Moreover, the cell death platform could be instrumental as a steppingstone to make cell death an Emerging Frontline Research Domain.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Co-promoter: Augustyns Koen
• Co-promoter: D'Haese Patrick
• Co-promoter: Van Der Veken Pieter

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Neuroblastoma (NB) is the most common solid tumor outside the brain of infants and very young children. The aggressive forms of neuroblastoma are often accompanied by an increased resistance to current chemotherapies due to defects in the molecular mechanisms that normally leads to the death of cancer cells. Therefore, the challenge is to find new molecular mechanisms to kill the cancer cells. Recently, we discovered a new approach to kill aggressive therapy-resistant neuroblastoma in mice by triggering a sort of biological rusting in cancer cells called ferroptosis. Ferroptosis rusts away the membranes of cells, which quickly kills the cells. By using nanoparticles, we were able to minimize the side effects of treatment and enhanced tumor targeting. However, to get full tumor regression without relapse using a nanomedicinal approach, it is needed to further improve the efficacy of ferroptosis targeting in neuroblastoma. In this project, we will use different genetic and pharmacological approaches to improve the therapeutic applicability of ferroptosis in neuroblastoma. We will identify potent ferroptosis triggers and nanoparticles, which could effectively suppress the tumor growth and relapse in cell- and patient-derived mouse cancer models as a stepping stone to clinical investigation.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Fellow: Hassannia Behrouz

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Unprotected iron can rust due to the attack of oxygen. Similarly, in our body, oxidative stress can kill cells in an iron-dependent way, which can give raise to organ injury or degeneration. This newly discovered type of cell injury or necrosis is referred to as ferroptosis. The study of how this type of cell death works at the molecular levels gains a lot of interest, due to its assumed high clinical relevance. On the one hand, our research focusses on using ferroptosis or 'biological rust' to eradicate cancer such as neuroblastoma using nanomedicinal approaches. On the other hand, blocking ferroptosis using small compounds is intensively investigated in an attempt to interfere with e.g. acute organ failure in intensive care patients or patients with chronic degenerative diseases. This work is imbedded in an interdisciplinary approach and occurs in collaboration with experts and physicians in the field.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Fellow: Goetschalckx Ines
• Fellow: Veeckmans Geraldine

Research team(s)

• Pathophysiology

Project type(s)

• Research Project

Abstract

Unprotected iron can rust due to the attack of oxygen. Similarly, in our body, oxidative stress can kill cells in an iron-dependent way, which can give raise to organ injury or degeneration. This newly discovered type of cell injury or necrosis is referred to as ferroptosis. The study of how this type of cell death works at the molecular levels gains a lot of interest, due to its assumed high clinical relevance. On the one hand, our research focusses on using ferroptosis or 'biological rust' to eradicate cancer such as neuroblastoma using nanomedicinal approaches. On the other hand, blocking ferroptosis using small compounds is intensively investigated in an attempt to interfere with e.g. acute organ failure in intensive care patients or patients with chronic degenerative diseases. This work is imbedded in an interdisciplinary approach and occurs in collaboration with experts and physicians in the field.

Researcher(s)

• Promoter: Vanden Berghe Tom
• Fellow: Vanden Berghe Tom

Research team(s)

• Pathophysiology

Project website

Project type(s)

• Research Project

Abstract

Researcher(s)

• Promoter: D'Haese Patrick
• Promoter: Vanden Berghe Tom

Research team(s)

• Pathophysiology

Project type(s)

• Research Project