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The Department of Physiology at VU University Medical Center studies (patho)mechanisms of the cardiovascular system. Our research projects focus on diastolic heart failure, inherited (cardio)myopathies, strategies to improve tissue reperfusion and prevent vascular dysfunction in various clinical pathologies (sepsis, diabetes). The majority of our research projects is performed in collaboration with investigators from other (clinical) departments, in close collaboration with the Institute for Cardiovascular Research ICaR-VU.
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Diastolic heart failure: To unravel pathophysiological mechanisms underlying diastolic dysfunction, in vivo clinical studies are combined with cellular studies in human cardiac preparations.
Cardiovascular ageing: The main focus of the research in the lab is ageing of the cardiovascular system. This is the main risk factor for cardiovascular disease and we are interested in the role of so-called non-coding RNA in this process.
Heart failure: Molecular changes that underlie cardiac muscle function, hypertrophy and hypertrophic cardiomyopathy.
Heart failure: The energetics of mechanical overload in heart and skeletal myocytes.
Skeletal muscle myopathies and atrophy: The unifying theme of our research concerns the regulatory and pathogenic role of myofilament proteins in muscle contraction, with special focus on the diaphragm.
Sarcomeric Proteins: Origin of the alterations in contractile properties and energy utilisation by the mitochondria of cardiac muscle cells during heart failure; origin of skeletal muscle weakness resulting from alteration in cytoskeletal muscle proteins.
Atrial fibrillation: Our studies focus on normalization of protein homeostasis to reverse structural remodeling and restore cardiomyocyte function in AF.
Impairment of organ perfusion in metabolic disease: Impaired organ perfusion in obesity and type 2 diabetes, and to translate this knowledge into prevention of type 2 diabetes and associated vital organ failure.
Circulation and vasculature: Our research on blood vessels focuses on (i) the molecular mechanisms that control vascular permeability and (ii) the biomechanics that drive vascular function and remodeling, at the level of arteries, arterioles and veins as well as the level of endothelial and smooth muscle cells
Cardiac and skeletal muscle: Thyroid-hormone regulated gene expression in cardiac and skeletal muscle.
Circulation and vasculature: The effect of chronic hypoxia on endothelial cell functions and endothelial cell progenitor differentiation/outgrowth in relation to vascularization of tissue-engineered tissue constructs
Cardiac and skeletal muscle: The mechanism of Dio3 induction and the role of reduced cardiac TH signaling in pathological gene expression and cardiac dysfunction in chronic heart failure.