Interrelations between Apoptosis and Autophagy in Autoimmune and Malignant Diseases

Abstract

The lifespan of a cell in the body oscillates between two fundamental processes, Autophagy, which ensures cell survival, even under conditions of cellular stress, and Apoptosis, which programs the end of cell life, not before the renewal of a new cell in a tissue. Overall, there is a continuation of daily life until a specified date of highlighting the length of the telomeres, in the chromosomal analysis of the cell. Apoptosis, in the scheduling of cell life, is a normal process which is different from cell necrosis that occurs as a result of physical or chemical aggression. The decision to activate a suicide process is made based on intrinsic or extrinsic apoptotic messages. The intrinsic inducers of apotheosis come from the mitochondria or nucleus. Extrinsic inducers of apotheosis are ligands, cytokines for death receptors, (DR-Death receptors) on each cell surface. Autophagy: is a homeostatic and catabolic processes that allows the sequestration and lysosomal degradation of cytoplasmic organs and proteins, important for maintaining genomic stability and cell survival. Autophagy is regulated by the Beclin 1 protein, which forms a complex with a class III enzyme, phospho-inoside 3-kinase (PI3K), and serves as a platform for the recruitment of other proteins critical for autophagosome formation. Conclusions: The most important regulatory mechanism in autoimmunity and oncogenesis process are death receptors, caspases, mitochondria, the Bcl-2 family proto-oncogenes and tumor suppressor gene P53. Pharmacological manipulation of autophagy for cancer prevention and treatment will depend on our ability to successfully recognize the functional status of autophagy in tumors, and the availability of specific autophagic modulators.