Autophagy is a catabolic trafficking pathway for bulk destruction and turnover 
of long-lived proteins and organelles via regulated lysosomal degradation. In 
eukaryotic cells, autophagy occurs constitutively at low levels to perform 
housekeeping functions, such as the destruction of dysfunctional organelles. 
Up-regulation occurs in the presence of external stressors (e.g. starvation, 
hormonal imbalance and oxidative stress) and internal needs (e.g. removal of 
protein aggregates), suggesting that the process is an important survival 
mechanism. However, the occurrence of autophagic structures in dying cells of 
different organisms has led to the hypothesis that autophagy may also have a 
causative role in stress-induced cell death. The identification within the last 
decade of a full set of genes essential for autophagy in yeast, the discovery of 
human orthologues and the definition of signalling pathways regulating autophagy 
have accelerated our molecular understanding and interest in this fundamental 
process. A growing body of evidence indicates that autophagy is associated with 
heart disease, cancer and a number of neurodegenerative disorders, such as 
Alzheimer's, Parkinson's and Huntington's diseases. Furthermore, it has been 
demonstrated that autophagy plays a role in embryogenesis, aging and immunity. 
Recently, it has been shown that autophagy can be intensified by specific drugs. 
The pharmacological modulation of the autophagic pathway represents a major 
challenge for clinicians to treat human disease.