Cardiovascular disease remains the number one cause of death, not only in the chronic human condition (cardiac infarction, heart failure, diabetes), but also in many acute traumatic hospital conditions (cardiac by-pass surgery, PTCI and acute myocardial infarction, cardiogenic shock, sepsis). Our research is directed at the understanding of the 1) mechanisms through which current novel succesfull diabetes medicine (SGLT2 inhibitors) reduce cardiovascular events (heart failure, diastolic dysfunction, cardiac infarction) and 2) crucial cellular mechanisms underlying death/survival programs of the heart cell in these acute traumatic hospital conditions conditions and at the development of treatments to push the cell death/survival programs into the direction of survival.

In our current models, with emphasis on its translation to the clinic and human condition (taking into account co-morbidities, drugs commonly used in human treatment and clinical relevant anesthetic regimens), we primarily focus on 1) unraveling of the working mechanisms of SGLT2 inhibitors, and 2) the decisive role that mitochondria play in the setting of cardiac death induced by periods of ischemia (lack of oxygen, blood flow). Attention is especially given to 1) empagliflozin, and 2) the glycolytic enzyme hexokinase II, of which its binding to mitochondria is highly regulated and is of paramount importance to protect mitochondria and thereby combat cardiac cell death in almost all of the above conditions.
 

 RESEARCH EMPHASIS ON:

A) THERAPY AGAINST INFARCT DEVELOPMENT, MITOCHONDRIA-MEDIATED CELL DEATH, AND INNATE IMMUNITY INVOLVEMENT

B) UNDERSTANDING INTERACTION BETWEEN DIABETES AND HEART FAILURE FOR THERAPY DEVELOPMENT

C) EXPERTISE CENTRE ON EX VIVO CARDIAC FUNCTION and METABOLISM (STABILE ISOTOPES) OF MOUSE HEARTS

D) EXPERTISE CENTRE FOR ANIMAL ANESTHESIA