title: Mille modis morimur: We die in a thousand ways.
abstract: Dying cells subjected to apoptotic programs are engulfed by neighboring cells or by professional phagocytes, without inflammation or immunological reactions in the tissue where apoptosis takes place. Apoptotic cells release danger-associated project signals to their neighbours, through different molecular patterns, stimulate antigen production and immune responses. Microenvironmental effects with several functional consequences indicate that cell death is a complex process and may take place in several ways. This idea is expressed by the title of the Special Issue and by the title of the guest editorial "Mille modis morimur" meaning that not only multicellular organisms, but also single cells may die in a thousand ways. This idea is demonstrated by the papers serving as examples for cell death. Apoptosis was induced by clary sage oil in Candida cells. Heavy metal (Gd) induced cell motility and apoptosis was found in mammalian cells. RNA oxidation enhanced the reversion frequency of apoptosis in yeast mutants. The frequency of apoptotic micronucleus formation increased in a concentration-dependent manner by methotrexate. The antioxidant coenzyme Q10 protected renal proximal tubule cells against nicotine-induced apoptosis. The synergy of 2-deoxy-D-glucose combined with berberine induced lysosome/autophagy. The mitochondrial apoptotic pathway could be regulated by glucocorticoid receptor in collaboration with Bcl-2 family proteins in developing T cells. Cylindrospermopsin induced biochemical changes led to apoptosis in plants. Mechanisms of stress seriously impacted the risk of apoptosis. Transcriptional control of apoptotic cell clearance was achieved by macrophage nuclear receptors. Finally, the clinical aspects of apoptosis-induced lymphopenia were reviewed in sepsis and other severe injuries. These examples not only support the view of many ways of cell death, but predict further potential ways to induce or reduce the risk of cell death.
authors.affiliation: Department of Biotechnology and Microbiology, University of Debrecen, 1 Egyetem Square, Debrecen, 4010, Hungary. bgaspar@unideb.hu.
authors.forename: Gaspar
authors.initials: G
authors.lastname: Banfalvi
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D001343:Autophagy / Q000235:genetics*; D002175:Candida / Q000235:genetics / Q000254:growth & development; D002465:Cell Movement / Q000187:drug effects / Q000235:genetics; D060833:Cellular Microenvironment / Q000235:genetics*; D006801:Humans; D019216:Metals, Heavy / Q000633:toxicity; D010084:Oxidation-Reduction / Q000187:drug effects; D010586:Phagocytes / Q000378:metabolism; D018805:Sepsis / Q000235:genetics / Q000473:pathology; D014451:Ubiquinone / Q000031:analogs & derivatives / Q000235:genetics
chemical_list: D019216:Metals, Heavy; D014451:Ubiquinone; C024989:coenzyme Q10
keywords: Anti-apoptosis; Clinical relevance; Induction of cell death; Mitochondrial pathway; Plant apoptosis