Cell death.

Cell death is a crucial process involved in a variety of biological mechanisms controlling development, homeostasis, and immune regulation of multicellular organisms and its imbalance is associated with numerous pathologies. According to the literature, it is undeniable that the field of cell death research has been continuously growing and novel cell death modalities have been also described. Cell death can be classified according to morphological criteria identifying modalities such as apoptosis, necrosis, autophagy, or death associated with mitotic catastrophe. Additionally, cell death can be identified on the basis of biochemical mechanisms which include, for instance, the activation of different class of proteases (proteases, nucleases, and caspases) and according to the presence of specific cell surface molecules or the release of soluble mediators (immunogenic or nonimmunogenic cell death). The field of cell death is so complex that The Nomenclature Committee on Cell Death (NCCD) has recently proposed unified criteria which define the different types of cell death, while providing recommendations facilitating the communication among scientists involved in this field. The main purpose of this special issue is to cover the field of cell death with themes focusing on pathways and mechanisms that specify active forms of cell death in health and disease. The topics therefore span apoptotic signaling networks (e.g., Bcl-2 family proteins, caspase control, novel molecular players of apoptotic control in immune regulation, and epigenetic regulation of apoptosis) and noncanonical cell death pathways, including necroptosis, pyroptosis, and autophagy, with a particular attention on the relationship between these mechanisms. More specifically, M. E. Morrison et al. describe a novel role for the proapoptotic protein Bim in modulating cellular functions such as migration and extracellular matrix protein expression in retinal endothelial cells and pericytes. This study therefore provides additional regulatory mechanisms linking apoptosis control to vascular function. M. Garg et al. focus on the regulation of apoptosis during the immune response. Their work highlights the role of the linker histone H1.2 trafficking in inducing T-effector lym-phocytes apoptotic response after cytokine withdrawal. They demonstrate the well-controlled association between H1.2 and the proapoptotic mitochondrial resident Bak following metabolic stress. M. N. Rossi and F. Antonangeli review our current knowledge of the role of long noncoding RNAs in apoptosis control. The authors highlight the altered expression pattern of specific lncRNAs in cancer cells when compared with normal cells and tissues. They also underline that overexpres-sion or downregulation of different long noncoding RNAs in specific types …