Our work aims at characterizing the role of mitochondrial dysfunction in cardiac diseases. Besides a long-standing interest in Ca+ homeostasis and permeability transition, more recently we focused our attention on mitochondrial sources of oxidative stress highlighting the role of monoamine oxidases.
As a major target of oxidative stress we characterized the oxidation of myofibrillar proteins linking mitochondrial dysfunction with contractile impairments in both cardiac and skeletal muscles.
