Marion Mussbacher

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Systemic knockout of adipose triglyceride lipase (ATGL), the pivotal enzyme of triglyceride lipolysis, results in a murine phenotype that is characterized by progredient cardiac steatosis and severe heart failure. Since cardiac and vascular dysfunction have been closely related in numerous studies we investigated endothelium-dependent and -independent(More)
Cardiac oxidative stress has been implicated in the pathogenesis of hypertrophy, cardiomyopathy and heart failure. Systemic deletion of the gene encoding adipose triglyceride lipase (ATGL), the enzyme that catalyzes the rate-limiting step of triglyceride lipolysis, results in a phenotype characterized by severe steatotic cardiac dysfunction. The objective(More)
Background Perivascular adipose tissue (PVAT) has been shown to be an important modulator of vascular function through release of both relaxing and contracting factors. However, the involvement of PVAT in development of endothelial dysfunction is not well understood, yet. We have recently demonstrated that mice lacking adipose triglyceride lipase (ATGL)(More)
Background Systemic knockout of adipose triglyceride lipase (ATGL), the rate-limiting enzyme of triglyceride catabolism, results in a murine phenotype characterized by progressive accumulation of lipids in the heart finally leading to lethal cardiac dysfunction. Since cardiac and vascular dysfunction are closely related we investigated endothelium-dependent(More)
Systemic deletion of the gene encoding for adipose triglyceride lipase (ATGL) in mice leads to severe cardiac dysfunction due to massive accumulation of neutral lipids in cardiomyocytes. Recently, impaired peroxisome proliferator-activated receptor α (PPARα) signaling has been described to substantially contribute to the observed cardiac phenotype.(More)
Background Adipose triglyceride lipase (ATGL) has been characterized as key enzyme of mammalian triglyceride catabolism. Mice with global ATGL deficiency were previously described to suffer from lethal cardiac dysfunction that originates from defective peroxisome proliferator-activated receptor alpha (PPARa) signaling in the heart. Experiments from our(More)
Colistin electrostatically interacts with lipopolysaccharides (LPS). Pre-clinical studies demonstrated beneficial effects of colistin on LPS-induced coagulation and fibrinolysis. The objective of this trial was to investigate the effects of colistin during experimental endotoxaemia. In this randomised, double-blind, placebo-controlled, crossover trial 16(More)
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