The research of our laboratory focuses on macroautophagy or simply autophagy, a catabolic process highly conserved among eukaryotes that is involved in the degradation of long-lived proteins, dysfunctional protein complexes and aggregates, dysfunctional and superfluous organelles, and intracellular pathogens. Cargoes targeted to destruction are sequestered by double-membrane vesicles called autophagosomes and delivered to lysosomes for turnover. The resulting metabolites are reused by the cell as either an energy source or building blocks for the synthesis of new macromolecules.

Autophagy plays a pivotal role in maintaining cellular and organismal homeostasis, as it is involved in the adaptation to stresses, quality control, metabolism regulation, cell development and differentiation, stemness maintenance, type II program cell death, tumor suppression and immunity. An impairment or defect in autophagy can result in severe pathologies such as neurodegeneration, myopathies, chronic inflammations, and some malignancies. Crucially, it has also been shown that autophagy is an effective therapy to prevent or cure diseases, including several neurodegenerative disorders, muscular dystrophies, and specific types of tumors.

In our laboratory, we investigate the mechanism of autophagy and its regulation, but also the proteins required for recognition and elimination of the various autophagy cargoes. This knowledge is of primary biological relevance and is key to be able to modulate autophagy for the benefit of human health. In this latter context, it is also crucial to understand the exact contribution of autophagy in the various physiological situations and pathological conditions. Therefore, our group is also studying the interplay between autophagy and viruses, and the role of autophagy in preventing neurodegeneration.