Age-dependent accumulation of damaged mitochondria promotes the deterioration of biological systems leading eventually to the development and progression of several age-related diseases. Therefore, mitochondrial homeostasis is tightly associated with cellular and organismal survival. Cells have developed an extensive repertoire of molecular pathways to restore mitochondrial function and promote stress resistance.. Mitochondrial selective autophagy, known as mitophagy, regulates the size and quality of the mitochondrial population during development and challenging conditions. Superfluous and/or dysfunctional organelles are engulfed by autophagosomes and are subsequently delivered for degradation in lysosomes. Mitophagic flux declines with age, while its induction promotes healthspan, extends lifespan and confers neuroprotection across diverse species, highlighting its pivotal role in the maintenance of cellular and tissue homeostasis. Our laboratory investigates the molecular mechanisms that regulate mitophagy under stress conditions and examine the impact of mitophagy deficits or up-regulation in several models of human pathologies. Moreover, our interests are focusing on necrotic and mitophagic cell death and their interplay between cellular metabolism and ageing. Finally, we are developing novel and versatile genetic tools for biomedical research.