Our laboratory researches the mammalian mitochondrial electron transport chain (MtETC) and H+-ATP synthase, which together constitute the oxidative phosphorylation (OXPHOS) system and is centered in understanding the role of mitochondria as major integrator of the cellular metabolism.

We are particularly interested in the role of the mitochondria in the development and homeostasis of the cardiovascular system and in enhancing its resilience and regenerative potential upon injury. Thus, we aim to understand the relevance of mitochondria and the OXPHOS system in the pathophysiology of the heart, including ischemia-reperfusion, heart failure and its electric activity. We also investigate the relevance of mitochondria on inflammation, obesity and vascular physiopathology. Finally, we are investigating the contribution of the mitochondrial genetics, and its role as organismal integrator of the metabolism, in allowing healthy aging and their impact.

We are implementing high-throughput strategies to catalogue the set of the genes whose products participate in the biogenesis and regulation of the OXPHOS system (which we call the OXPHOME). We are also determining the factors that regulate the structural organization of the electron transport chain and the role that this superstructural organization plays in the production of reactive oxygen species (ROS). This area is linked to our interest in the role of ROS as mitochondrial second messengers and to our aim to deconstruct the mammalian OXPHOS system into its functional components (electron transport, proton pumping and ATP synthesis). With the knowledge that we are acquiring, we aim to identify and modulate molecular targets and regulatory pathways to protect the cardiovascular system against disease by increasing its robustness and its regenerative capacity.