Recent Advances in Apoptosis and Autophagy

Dear Colleagues,

Cell loss and the progressive deterioration of organ and tissue function are among the main causes of aging-associated and autoimmune diseases. Autophagy and apoptosis are well-known conserved processes involved in cellular and tissue dismantling and renovation, and a proper cellular balance allows for the maintenance of health. However, the interdependence between these pivotal processes is still debated: does one activate or suppress the other? The formerly morphological classification of three types of programmed cell death, i.e., type I—apoptosis; type II—autophagy; and type III—necrosis, is now outdated. Different death mechanisms linked to aberrant metabolism; ischemia; inflammation; oncogenesis, called anoikis; efferocytosis; pyroptosis; and ferroptosis have emerged. In this complex scenery, molecular pathways based on caspase enzymes, receptor-interacting serine/threonine-protein kinase 1-3 (RIPK1-3), glutathione peroxidase 4 (GPX4) and the mechanistic target of rapamycin kinase (mTOR) play a crucial role. The constant exchange of knowledge between clinical and biological researchers regarding programmed cell death pathways and the use of natural or synthetic modulators of apoptosis (and related efferocytosis) and autophagy may lead to novel therapeutic opportunities.

To address the most recent advances in autophagy, apoptosis, and other cell death mechanisms in aging-related disorders, we are proposing this Special Issue that welcomes original articles, comprehensive reviews and/or perspective articles.

Dr. Alessandra Stacchiotti
Dr. Annalisa Cappella
Guest Editors

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