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What Do We Research?

Our research focuses on desmin as the main protein component of the cardiac intermediate filaments. The accumulation of cleaved desmin, as well as its misfolding, are hallmarks of cardiac dysfunction in numerous experimental models of heart disease as well as clinical specimens. The loss of cell ultrastructure arising from desmin cleavage in the highly organized cardiac muscle cell was proposed as a straightforward cause of contractile dysfunction. In addition, protein misfolding is emerging as a major contributor to the development of cardiovascular disease. We use a combination of cell and molecular biology, advanced biochemistry, experimental models of cardiovascular disease, and human samples to study how  the loss and gain of (toxic) function of desmin can be therapeutically targeted to preserve the function of the heart.


Ongoing Research Projects:

- Investigating Early Desmin Cytoskeletal Remodeling in Experimental Cardiac Hypertrophy

- Understanding the Mechanism of Desmin Aggregation Under Oxidative Stress

- Investigating the Potential Role of Desmin as a Therapeutic Target in Experimental Models of Chemotherapy-Induced Cartiotoxicity 

- New Analytical Methods to Study Protein Misfolding in the Heart

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Adult mouse cardiac myocytes isolated from mice injected with AAV-GFP 2 weeks prior

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