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.