More than 64 million people worldwide suffer from heart failure. The multiple mechanisms that lead to this disease and the factors that promote it are far from being understood. A better understanding of the pathophysiological causes of heart disease is essential to develop new, individualized forms of therapy and treatment methods. However, it is clear that co-morbid conditions drive myocardial remodeling in some heart failure phenotypes such as heart failure with preserved ejection fraction (HFpEF), promoting a systemic inflammatory state that contributes to endothelial dysfunction, oxidative stress and modulation of diastolic function. Our recent results allowed us to formulate a comprehensive hypothesis describing how inflammation and oxidative stress affect myocardial dysfunction in heart failure (HF).
Our group aims to unravel the biological mechanisms underlying the stiffening of heart tissue that can lead to heart failure. We are using the knowledge gained from our recent discoveries to investigate novel treatment options for the condition. Our work employs a more refined approach than has ever been trialled before, based on an understanding of the variable factors involved in each case of heart failure.
Our recent discoveries involve oxidative stress and inflammation as a paradigm to the development of heart disease. The co-morbidities present with the condition raise levels of pro-inflammatory proteins in the blood and drive inflammation of cardiac vasculature. This disrupts signalling between the endothelial cells that line the small blood vessels within the heart muscle, cardiomyocytes and fibroblasts. Changes to any of these properties can be altered in heart disease and contribute to the diastolic stiffness characteristic of HFpEF. The aim of our proposed research is to deepen our basic understanding of heart failure and in particular HFpEF pathophysiology associated with comorbidities, age and sex differences, in order to provide firm foundations for clinical innovation. Our research team together with our national and international collaborators focus on working towards developing these specialised therapeutic approaches.
Our future tasks are to establish a program for translational cardiac research at RUB. The program will strengthen our vision of a physiology-oriented approach to treatment and pave the way for more innovative diagnostics and individualized therapies. The program aims to translate our findings from the research lab to clinical development, that is, from bench-to-bedside. In the same way, observations and questions from clinical practice should flow back into the lab - from bedside-to-bench.
Our group is bridging between basic research and clinical application, bridging the gap between cardiovascular biology and therapeutic intervention. We would like to take a more in-depth look at the basic pathophysiology of heart failure overall. Building on understanding of the interplay between inflammation, oxidative stress and heart failure, we hope to develop more effective treatment options and drugs for patients with existing heart problems and comorbidities. We are particularly interested in reducing cardiovascular deaths among socially disadvantaged people and ethnic minorities.
Our research is conducted at the Dept. of Cellular and Translational Physiology, Institute of Physiology at Ruhr University Bochum and Institute for Education and Research (Institut für Forschung und Lehre, Molecular and Experimental Cardiology) Katholisches Klinikum Bochum, St.Josef Hospital. Most instrumentation and laboratory equipment required to successfully conduct the project is available in the laboratory. Our laboratory has an established track record in cardiac muscle research and especially in titin biology, in heart failure, oxidative stress, inflammation, signalling pathways, protein modifications and post-translational modifications, in vitro and in vivo studies. Our collaborations are all well-established national and international.
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Last update: Jan 20, 2025