BRFAA - Biomedical Research Foundation Academy Of Athens
Biomedical Research Foundation Academy Of AthensAcademy Of Athens


Capetanaki’s laboratory studies the mechanisms responsible for heart failure development and investigate potential strategies for its prevention.

Heart failure is a world-wide public health problem and the leading cause of mortality. The molecular and cellular mechanisms underlying heart failure remain elusive. Cardiomyocyte death is considered a major cause in the development of dilated cardomyopathy and heart failure, possibly due to disturbance of the cytoskeletal network (desmin etc ) that extends throughout the cell and links the contractile apparatus, through the z-disc, to the nucleus and nuclear matrix, to mitochondria and perhaps other organelles, and through sarcolemma to the extracellular matrix. Disturbance in several members of this network leads to the same disease, that is dilated cardiomyopathy and heart failure. A major part of Capetanaki’s research has focused on the elucidation of the mechanism by which perturbations in the cytoskeleton, and most specifically deficiency in the muscle specific intermediate filament protein desmin leads to mitochondrial defects and cardiomyocyte death. For this purpose, we follow two strategies: One will address the cardiomyocyte intrinsic molecular and cellular mechanisms leading to mitochondrial defects, cell death and heart failure and the second will elucidate the contribution of extrinsic factors (including inflammation) in the progress of the disease. These efforts have already opened very promising paths towards not only our better understanding of the function of desmin in cardiomyopathy but furthermore, the development of strategies to reverse this process.

The majority of Ph.D. candidates and post-doctoral fellows who have joined Capetanaki’s laboratory (see figures below) have being working on the unraveling of the mechanisms of heart failure development and protection.

Schematic representation of the intermediate filament (IF) scaffold (yellow) in cardiac muscle and its potential associations with different membranous compartments and organelles including the nucleus, mitochondria, lysosomes and potentially the sarcoplasmic reticulum (SR). Mutations causing DCM are shown with black stars (*) while those causing ARVD/C with blue (*) (adapted from Capetanaki et al., 2007)