Molecular Cardiology Research Group

Prolonged pathological stress, such as chronic pressure overload or myocardial infarction, has been demonstrated to cause maladaptive cardiac growth, which ultimately results in heart failure. Despite notable advancements in heart failure therapy over recent decades, the condition persists as a significant public health concern. In contrast to pathological stress, the heart demonstrates the capacity to adapt and maintain cardiac function in response to exercise training. It is of particular importance to note that physiological cardiac adaptation differs from adverse ventricular remodeling in both its structural and molecular characteristics. Gaining insight into the cardioprotective signaling pathways activated in an athlete's heart presents a promising opportunity for the development of novel treatments for heart failure. It is our intention to translate the findings of preclinical studies, including in vitro and ex vivo models, as well as in vivo small- and large-animal models, into clinical applications. Additionally, we seek to utilize clinical observations to gain mechanistic insights. The primary focus of our preclinical studies is on the following areas: The identification of novel cardiokine systems, including adrenomedullin, apelin, apela, and endothelin-1, is a key objective, [i] those that regulate cardiac contractility, coronary circulation, metabolism, ventricular remodeling, and cardiac regeneration; [ii] The discovery of new cardiokine regulators of cardiac fibrosis; [iii] The exploration of the interactions between microRNAs, long non-coding RNAs, and mRNAs that influence ventricular remodeling; [iv] The development of innovative small-animal models of myocardial infarction and heart failure; and [v] The identification of exerkines that regulate exercise-induced adaptations in cardiac and skeletal muscle. The primary objectives of the clinical studies are as follows: [i] The identification of novel biomarkers (such as cardiokines, microRNAs, and long non-coding RNAs, etc.) with tissue specificity in acute myocardial infarction and heart failure is a primary objective. [ii] The development of novel reperfusion therapies to improve myocardial salvage in patients afflicted with myocardial infarction is a secondary objective. In regard to the research basis, the group offers the following professional services to its participating partnerships: The group is engaged in the development of novel small- and large-animal models of heart failure, as well as cardiac PET-MRI studies in large-animal models of heart failure and the testing of novel lead compounds in small- and large-animal models of heart failure.