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Autophagy (literally “self-eating”) and apoptosis (programmed cell death) control the turnover of various cytoplasmic constituents within eukaryotic cells, and of cells within organisms, respectively. Autophagy is triggered under certain hostile conditions such as nutrient starvation, hypoxia, immune and hormone stimulation. Generally autophagy blocks the induction of apoptosis, and apoptosis-associated caspase activation shuts off the autophagic process. However, in special cases, autophagy or autophagy-relevant proteins may help to induce apoptosis or necrosis. The interaction between autophagy and cell death pathways influences the normal clearance of dying cells, as well as immune recognition of dead cell antigens. Therefore, the disruption of the relationship between autophagy and apoptosis has important pathophysiological consequences. Many researches show that malfunctions in this process are related to diseases such as cancer, neurodegeneration, diabetes, autoimmune and cardiovascular disease.
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