Link to Mahmoud Abdellatif’s Research Group Website

Our group is focused on investigating the molecular and cellular mechanisms of ageing in the cardiovascular system and how they can be targeted to prevent, delay or even reverse prevalent age-related cardiovascular disorders. We are particularly interested in heart failure with preserved ejection fraction, which is a leading cause of hospitalization and mortality among the elderly with limited therapeutic options. To address this knowledge gap, we have developed diagnostic tools and innovative experimental therapies. Some of these therapies, including spermidine, are currently being tested in randomized human trials.

Link to Christoph J. Binder’s Research Group Website

Our group is investigating immune mechanisms of atherosclerosis with a special focus on the role of innate and humoral immunity and how this can be exploited for the treatment of cardiovascular disease. Our laboratory discovered the importance of humoral immune responses targeting so-called oxidation specific epitopes (OSE), which are generated by lipid-peroxidation and are present on oxidized LDL, dying cells and extracellular vesicles. We are interested in defining the binding properties of these humoral immune components, which include natural IgM antibodies and certain complement components, and the molecular mechanisms by which they function in both physiology (clearance of apoptotic cells) and pathophysiology (vascular inflammation, thrombosis). Another major aspect of our work focuses on the role of cytokines in atherosclerosis, where we discovered the protective role and mechanisms of several cytokines.

Link to Stefan Coassin’s Research Group Website

Our group is interested in addressing challenging genetic targets and navigating complex genomic regions using advanced molecular genetic techniques. The main focus is on understanding the genetic regulation of the Lipoprotein(a) trait and the role of genetic variation in the LPA KIV-2 copy number region. Additionally, we enjoy exploring the potential of nanopore sequencing and other emerging genetic technologies to tackle tough questions across disciplines.

Link to Thomas Felder’s Research Group Website

Our research on human lipid metabolism provides a basis for improved understanding of common diseases associated with obesity. Lipids perform a variety of functions in cellular metabolism, are components of cell membranes and play an important role in cellular communication and the formation and dissolution of inflammatory processes. In cells, free fatty acids are metabolized to complex and neutral lipids for protection from toxic effects (lipotoxicity), the latter being stored in LDs. Chemicals, medicines and hypercaloric diets can promote the storage of fat and the number or size of LDs. However, excessive LD accumulation in liver cells can contribute to the progression of chronic diseases such as metabolic associated fatty liver disease (MAFLD) and cancer. We characterize various lipidomes in humans and model organisms to better understand lipid associated diseases.

Link to Sasa Frank’s Research Group Website

1. Identification of new prognostic biomarkers in patients with acute heart failure (AHF). We have recruited two independent cohorts (AHF1; N=152 and AHF2; N=315) of patients with AHF. We use NMR-metabolomics, MS-lipidomics, and targeted measurements of the potential molecular and functional biomarkers and evaluate their prognostic utility using appropriate statistical methods.
2. Differences in molecular fingerprints and vascular function between healthy subjects (HS; N=65) and patients with metabolic syndrome (MS; N=65)). We examine differences between healthy subjects and patients with MS, regarding relationships between indicators of vascular function (FMD, NMD), metabolites, and oxidative stress biomarkers.
3. Molecular characterization of COVID-19 patients with (n=130) and without overlapping pneumonia (n=120). We examine whether overlapping pneumonia affects the associations between clinical characteristics and molecular fingerprints in COVID-19 patients.

    Link to Dagmar Kratky’s Research Group Website

Lipid storage and degradation are tightly regulated processes involving intracellular lipid hydrolases, enzymes of lipid biosynthesis, and regulatory proteins. An excessive lipid accumulation is central in the pathogenesis of prevalent metabolic diseases (e.g. obesity, diabetes, atherosclerosis). Our team investigates the function of lipid hydrolases in the regulation of lipid and energy metabolism in the whole organism, specific organs, and distinct cells. We are also interested in the role of lipid hydrolases in macrophages with regard to atherosclerosis development.

Link to Claudia Lamina’s Research Group Website

The Statistical Genetics group focuses on the implementation and application of (new) statistical methods to analyze and evaluate the genetic basis of diseases. These statistical methods include Genome-wide association studies, genetic risk scores, causal inference and Mendelian Randomization, nonlinear modelling and survival analysis. We are primarily interested in atherosclerosis-related traits, like lipoprotein(a), lipids, obesity, Type 2 Diabetes, peripheral arterial disease and cardiovascular diseases.

Link to Marion Mussbacher’s Research Group Website

The main research focus of the Mussbacher lab lies in understanding the complex interplay between inflammatory and metabolic signals that shape obesity-related diseases such as atherosclerosis and fatty liver diseases. We aim to understand how (1) platelets modulate metabolic signaling circuits such as endoplasmic reticulum stress and how (2) adipose tissue locally (via paracrine signaling of perivascular adipose tissue [PVAT]) and systemically (via lipolysis-dependent fatty acid release) modulates cardiometabolic diseases.

Link to Selma Osmanagic-Myers’ Research Group Website

In modern societies with increasingly older populations, age is becoming a major risk factor for atherosclerosis development. However, the underlying molecular mechanisms, especially with regard to the aging of the innermost blood vessel layer, the endothelium, are still not fully understood. Our team investigates how cellular aging (senescence) of endothelial cells and other cardiovascular cell types affects development of chronic diseases such as atherosclerosis and cardiovascular disease. We utilize different premature aging models resembling Hutchinson-Gilford progeria syndrome (HGPS) in the rodent system as well as in human system using iPSCs derived from HGPS patients. Our ultimate goal is to “unclog” the aged blood vessels and promote development of the healthy vasculature.

Link to Andreas Ritsch’s Research Group Website

Our research is focused on the implication of lipid and lipoprotein metabolism on the development of cardiovascular diseases. We are interested in the role of reverse cholesterol transport in this scenario. Our research work is encompassing basic research, animal-based studies as well as clinical studies and is targeting the development of new strategies for prevention and therapy of atherosclerotic diseases in humans.

Link to Susanne Sattler’s Research Group Website

Our research focusses on the cellular and molecular interplay between the immune system and the cardiovascular system. We investigate the role of the adaptive immune system in maintaining myocardial health and during the acute and chronic immune response following injury to the heart, such as after a myocardial infarction. In addition, we investigate autoimmune mechanisms developing during coronary artery disease and if these predispose patients to worse outcome. Our goal is to target the immune system for new therapeutic options in cardiology, e.g. to better predict, treat and possibly prevent the development of heart failure.

Link to Johannes’ Schmid Research Group Website

Our research interests focus on various aspects of inflammation and how acute as well as chronic inflammatory processes are involved in various diseases, such as cancer or cardiovascular diseases. We are investigating signaling molecules of the NF-κB pathway, which plays a central role in the control of inflammation. Different experimental systems are used, such as cell culture and mouse models (including primary human endothelial cells from arteries or veins, TERT-immortalized cells, cancer cell lines, as well as mouse models with cell-type specific chronic inflammation). We perform atherosclerosis models, platelet function assays and high-end microscopy. The results are then compared with data from patients or healthy humans and analyzed by professional bioinformatics and pathway- or network-analysis.

Link to Martina Schweiger’s Research Group Website

Our research focuses on the vivid intercellular communication between adipocytes and non-adipocyte cells and how it affects adipocyte metabolism, adipose tissue metabolic flexibility and ensures tissue homeostasis under physiological conditions like fasting and cold-exposure but contributes to the pathophysiology of aging or cancer-associated cachexia. At the center of the cachexia syndrome is the cachexigenic tumor, however, the differences between cachexigenic and non-cachexigenic cancers is yet not known. To address this question, we are currently studying cellular and metabolic differences between cachexigenic and non-cachexigenic cancer cells and tumors and how the tumor- lipid- and -immune microenvironment changes its metabolic- and secretory profile to alter host tissue metabolism as well as anti-tumor-therapy.

Link to Simon Sedej’s Research Group Website

Our research focuses on the fundamental mechanisms of cardiac aging and heart failure with preserved ejection fraction (HFpEF) – the most common and still growing chronic cardiovascular disease in the elderly. In the Cluster of Excellence ‘MetAGE’, we aim to validate caloric restriction mimetics as effective molecular candidates and therapeutic interventions against cardiovascular aging, cardiometabolic syndrome, and HFpEF. We combine whole body physiological and cell-/tissue-specific molecular approaches by using aged or appropriate transgenic animal models and human liquid and myocardial biopsies from failing and non-failing donors.

Our new flagship projects INTERACD⁺ and VASC-HEALTH, respectively, concentrate on the mechanisms responsible for exercise- and NAD⁺-mediated protection from cardiometabolic risk and aim at defining actionable mechanistic targets based on autophagy and vascular attrition, which are so far not amenable to therapeutic interventions.

Link to Walter Speidl’s Research Group Website

Clinical lipid therapy in patients with coronary artery disease, heterozygous familial hypercholesterolemia and elevated lipoprotein(a) levels. Relation of disease state, genetic mutations, lipid levels and inflammatory activation.

Link to Herbert Stangl’s Research Group Website

The HDL metabolism is still less understood compared to LDL metabolism as it is more versatile with regard to cholesterol transport and the receptors involved. The transport of cholesterol by HDL from the periphery back to the liver for disposal is called reverse cholesterol transport. The atheroprotective effects of HDL are complex, besides its role in cholesterol removal from the periphery HDL binding can initiate signaling cascades thereby affecting a multitude of metabolic targets. HDL mediates lipid transfer by several different mechanism (selective uptake, cholesterol efflux / exchange, particle uptake). Our team investigates the contribution of the different transfer routes for lipid transfer using model cells systems ranging from cell lines like HepG2 to human liver organoids. For the examination of lipid trafficking techniques with nanometer resolution are applied.

Link to Ivan Tancevski’s Research Group Website

Macrophage biology, Kupffer cell biology, Reverse Cholesterol Transport, LDL cholesterol uptake

Link to Oksana Tehlivets’ Research Group Website

Methylation next to phosphorylation is an important regulatory mechanism. Homocysteine is an evolutionary conserved master regulator of methylation. It is also an independent risk factor of atherosclerosis, increases cardiovascular risk in combination with cholesterol, is linked to cardiac pathology and is a strong predictor cardiovascular mortality. Using different model organisms, we aim to understand how homocysteine-associated deregulation of methylation alters cellular function in particular lipid metabolism and how it contributes to the development of cardiovascular disease. We expect that elucidation of methylation-dependent mechanisms triggered by homocysteine will improve understanding of risk factors of cardiovascular disease.

Link to Dimitris Tsiantoulas’ Research Group Website

Heart attacks are the main cause of death worldwide. The main underlying pathology of this devastating condition is atherosclerosis, a lipid-driven chronic inflammatory disease that leads to the formation of atherosclerotic plaques in large and medium size arteries.  Plaque rupture or erosion triggers thrombus formation, which restricts blood flow in the artery, thereby limiting oxygen supply to the heart muscle and consequently causing myocardial cell necrosis. Dimitrios Tsiantoulas leads a research group that studies the role of the immune system in cardiovascular diseases, including atherosclerosis and myocardial infarction, and lipid metabolism.