Autophagy

Abstract

Autophagy is a conserved proteolytic mechanism that degrades cytoplasmic material including cell organelles. Although the importance of autophagy for cell homeostasis and survival has long been appreciated, our understanding of how autophagy is regulated at a molecular level just recently evolved. The importance of autophagy for the quality control of proteins is underscored by the fact that many neurodegenerative and myodegenerative diseases are characterized by an increased but still insufficient autophagic activity. Similarly, if the cellular stress, leading to deoxyribonucleic acid (DNA) damage, mitochondrial damage and/or damaged proteins, does not result in sufficient autophagic repair mechanisms, cells seem to be prone to transform into tumour cells. Therefore, autophagy has multiple roles to play in the causation and prevention of human diseases. Key concepts: Autophagy is a cellular stress response induced to ensure cell survival, but excess autophagy may lead to cell death. The kinases TOR (target of rapamycin) and PI3K (phosphatidyl inositol 3 kinase) are two essential components of the autophagy molecular machinery. The family of genes or proteins called Atg (for a u t opha g y related) comprises the core of the molecular machinery of autophagy. Upon autophagy induction the enwrapped cytoplasmic components and organelles are recycled by degradation in the autolysosome. Autophagy can be dysregulated and may contribute to many pathologic processes.