We are interested in understanding the connection between aging and the malfunctioning of a cellular process involved in cellular quality control known as autophagy. All the cells in the human body have surveillance systems that detect and eliminate damaged structures and toxic products. Our working hypothesis is that these surveillance mechanisms, including autophagy, become defective as organisms age and this results in accumulation of damage inside cells, which often leads to their functional failure and death. The ultimate goal of our studies is to devise interventions to repair or restore normal autophagic activity in old organism to increase the healthy years of life and, potentially, longevity.
Autophagy, or the degradation of intracellular components in lysosomes, is tightly connected with food intake and the overall nutritional status. In fact, fasting is associated with activation of cellular cleaning through lysosomes. In contrast with the exhaustive molecular characterization that have been made through the years of the signaling mechanism that participate in nutrient sensing, we have limited insights on how these signals are integrated at the lysosomal compartment.
We are currently focusing in gaining insights on the connection between one of the important food sensors in the cell (mTOR) and lysosomes. Understanding the molecular players that participate in this process should help future efforts to design drugs to enhance cellular homeostasis and consequently improve organ function in the elderly, as well as delay onset of age-related diseases such as neurodegenerative and metabolic disorders.