Heart disease is the number one cause of death in Europe and the world. Cardiac remodeling involving cardiac hypertrophy is associated with higher morbidity as well as mortality due to heart disease. Cardiac muscle mass is potentially influenced by the ubiquitin proteasome system (UPS). At the heart of the UPS is the proteasome, which specifically degrades targeted proteins into peptides. The candidate has identified that the cardiac proteasomal core, the 20S proteasome, is a heterogenic group of highly similar multiprotein complexes with different functionality. During the development of cardiac hypertrophy, the assembly and thus the composition of 20S proteasome complexes is distinctly regulated. In consequence, proteasomal activities change non-uniformly. The objective of the proposed study is to analyze the impact of this regulatory mechanism on cardiac remodeling.
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