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Brown fat thermogenesis and metabolic health

Thermogenic adipocytes are a remarkable type of metabolic cell. These UCP1-expressing cells are activated by cold and use energy-dense nutrient such as fatty acids, carbohydrates, and derived carbohydrates for producing heat to maintain body temperature homeostasis. Activation of thermogenic adipocytes has been shown to improve metabolic health in regular rodents, preclinical animal models of metabolic disease and humans. Thermogenesis is a process that depends on the environmental temperature and the physiognomy of the animal. Hence the thermogenic activity greatly varies from warmer to colder season as well as differs from mice to men. Our goal is to understand how thermogenic adipocytes adapt their metabolism to the extreme challenges of high metabolic flux, high oxidative activity, as well as synthesis of new organelles and cellular structural remodeling.


Adipose tissue inflammation and metabolic disease

Adipocytes are key regulators of metabolic health: healthy white adipocytes are essential as in the complete absence of white adipose tissue in mice and humans systemic metabolic homeostasis is compromised. In the very different condition of obesity, excess accumulation of white adipocytes leads to the same phenotypic alterations of metabolic disease. Obesity is a chronic inflammatory disease and adipocytes are actively recruiting professional immune cells with chemokines when they are stressed. Interestingly, white adipose tissue inflammation is both required for the development of healthy fat cells but also contributes to their dysfunction in obesity. Our goal is to define molecular mechanisms of adipocyte health that direct the nature of adipose inflammation and associated systemic pathologies such as diabetes and atherosclerosis.


Cardiomyocyte adaptation in myocardial infarction

The heart is a fascinating and dynamic organ essential for human life. However, its metabolic flexibility is compromised in many critical medical conditions such as cardiohypertrophy, heart failure and during myocardial infarction. Both physiological changes in heart rate as well as the very distinct condition of heart disease require special mechanisms of adaptation. This is even more apparent in light of the unique structural features of myocyte organelles, particularly the endoplasmic reticulum and mitochondria. Like in other conditions of metabolic disease, heart disease has s strong inflammatory component, both for healthy as well as maladaptive regeneration and tissue scarring. Our goal is to understand the molecular adaption of a trained heart versus dysfunctional heart, particularly after myocardial infarction. A detailed molecular understanding of cardiomyocyte-immune cell interaction would be transformative for designing new therapeutic strategies of myocardial infarction outcomes.

Shivering, exercise and skeletal muscle function

Next to age and genetic predisposition, physical activity and exercise are the most important factors for maintaining a healthy metabolism throughout life. Also, even as a therapeutic life style intervention, exercise or mild physical activity have beneficial effects on cardiometabolic health. Surprisingly, we know very little about how skeletal muscle cells control the change in metabolism during the transition from sedentariness to physical activity and such knowledge would be critical for developing molecular therapies in support of life style changes or vice versa. Somewhat paradoxically, in other severe myopathies, such as muscle wasting in immobilized subjects or cancer cachexia, similar metabolic alterations take place as in beneficial exercise but the underlying mechanisms remain elusive. Our goal is to identify novel regulators of skeletal myocyte adaptation, and explore how these relate to physical activity and metabolic disease.






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Munich Heart Alliance





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