In cooperation with several pediatric cardiac surgery centers, we have set ourselves the goal of finding out which materials are optimal for the correction of congenital heart defects. Unfortunately, clinical experience shows that some of the materials used change over time and have to be replaced during a second surgical procedure. For this reason, we examine the materials of various origins obtained in the operating theater histologically and immunohistochemically in order to reconcile the findings with the clinical data of the patients in a second step. This enables us to bridge the gap between experimental research and everyday clinical practice. Furthermore, we can identify indicators that show any "wear and tear" of implanted material. In this way, the materials are not only assessed in terms of their quality and longevity, but are also used to detect changes at an early stage and initiate preventive measures in good time.

Atrial fibrillation is one of the major health economic challenges in Western countries in the coming years. It is one of the most common arrhythmias in adults and increases the risk of stroke, heart failure, hospitalization and death. Due to the rising average age of the population, a sharp increase in the expected number of patients with atrial fibrillation is predicted. During the pathogenesis of atrial fibrillation, extensive structural, electrical and metabolic remodeling processes (so-called atrial remodeling) take place in the atria. These processes can precede the arrhythmia or be induced by it. This atrial remodeling is thought to play a role in both the initiation and maintenance of the arrhythmia, and current guideline-based pharmacotherapy is aimed at rhythm control and maintenance as well as anticoagulation to prevent complications. In addition, in interventional therapy approaches, areas that are considered to be the starting point for atrial fibrillation are either sclerosed, isolated or surgically removed. Therapeutic approaches to delay atrial remodeling do not yet exist. In our research project, we isolate primary cardiomyocytes from atrial tissue and investigate intracellular Ca2+ dynamics and cell shortening with the help of fluorescence microscopy and camera-based methods. In cooperation with the Institute of Pharmacology we hope to gain new insights into the pathophysiology of atrial remodeling and to create starting points for possible therapies.

SGLT2 is a sodium/glucose cotransporter that has become particularly well known for its function in the kidney. There, in the first two segments of the proximal tubules, it takes over the reabsorption of approx. 90% of the glucose filtered by the kidney. In patients with diabetes, the expression of SGLT2 is upregulated, which leads to an increased glucose renal threshold. These basic principles led to the approval of SGLT2 inhibitors for the treatment of type 2 diabetes in 2012. SGLT2 inhibitors are derived from the natural glycoside phlorizin and block SGLT2. This leads to increased excretion of glucose via the urine and an associated reduction in blood glucose levels. In addition to the benefits for patients with diabetes, studies have shown that the use of SLGT2 inhibitors has a positive effect on the cardiovascular system. Large-scale studies with cardiovascular endpoints showed that hospitalization rates due to heart failure decreased, cardiovascular mortality decreased and cardiac structure and function improved significantly with the use of SGLT2 inhibitors. However, the molecular mechanisms underlying these observations are still insufficiently investigated and form the basis of this research project.