Die Vortragsreihe Medizinische Forschung der Medizinischen Fakultät OWL findet im Semester (außer in den Schulferien) mittwochs um 17:00 Uhr (~1Std.) statt.

Ziel der Veranstaltung ist der Austausch und die Vernetzung der Forschenden und Forschungsinteressierten im Bereich der medizinischen und medizinrelevanten Forschung.

Forschende der Medizinischen Fakultät OWL, der drei Krankenhausträger, die gemeinsam das Universitätsklinikum OWL bilden (Evangelisches Klinikum Bethel, Klinikum Bielefeld, Klinikum Lippe) sowie forschungsinteressierte niedergelassene Ärzt*innen in OWL präsentieren Ihre aktuellen Forschungsprojekte und tauschen sich zu Ihrer Forschung und neuen Projektideen aus. Kolleg*innen anderer Fakultäten, dem HDZ sowie nationaler und internationaler Institute sind als Redner*innen und/oder Diskutant*innen ebenfalls herzlich willkommen.

Abstract des Vortrags:

Immune cell responses in cardiometabolic diseases – impact of brown adipose tissue

Brown adipose tissue (BAT), historically known for its role in thermogenesis, has recently gained attention not only as a promising target for the treatment of obesity, but also as a modulator of cardiovascular health. Mechanistically, BAT regulates lipid and glucose homeostasis and also serves as an endocrine organ by secreting systemically active hormones, so called batokines. The role of BAT has also been investigated in the context of myocardial ischaemia/reperfusion injury (I/R). Indeed, after I/R, activation of the sympathetic nervous system with massive catecholamine release has a direct effect on BAT activity. This strong BAT activation is mainly attributed to cardioprotective effects, interestingly not only in preclinical models, but also in humans. The secretory capacity of BAT was found to be primarily responsible for the cardioprotective effect. However, our own studies further indicate the crucial role of BAT in the modulation of inflammatory reactions after I/R. Indeed, BAT seems to dampen inflammatory cell infiltration to the ischemic area thereby limiting scar size and left ventricular dysfunction. However, with the development of metabolic disorders, the positive and ani-inflammatory role of BAT is lost, resulting in an impaired immune response after I/R. The activation of BAT could therefore be a new therapeutic target for the regulation of a balanced immune response after I/R.