Mitochondrial function if a cornerstone of metabolic plasticity, allowing the eukaryotic cell to adapt efficiently to changing energetic demands and nutrient availability. Its role in human physiology is well documented and its dysfunction has been associated with an always increasing number of pathologies. In particular, mitochondria as a source of damaging ROS has been extensively investigated. Nevertheless, how mitochondria function or dysfunction contributes to disease development is still a matter of controversy.
In healthy individuals, mitochondrial activity is associated with low levels of mitochondrial ROS due to optimized electron transfer activities and the presence of high levels of antioxidants. In disease states, dysfunctional mitochondria produce high levels of ROS that cannot be detoxified efficiently leading to an oxidative stressed state.
We investigate the impact on tumor development, its role in the vascular complications of diabetes, in the pathological development of liver steatosis and in the toxicity associated with some pharmacological treatments. All these aspects are investigated at a molecular, cellular and physiological level.
We also aim to validate the application of biomarkers based on the evaluation of mitochondrial function in the diagnosis and prognosis of these diseases.
The particular contribution of gender is also considered, as well as the impact that the results may have on different social groups in the analysis of the data and on their communication.