Research Groups

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 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 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 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 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 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.