Galluzzi L, Vitale I, Abrams JM, Alnemri ES, Baehrecke EH, Blagosklonny MV et al.. Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012. Cell Death Differ 19:107-120

INSERM U848, Apoptosis, Cancer and Immunity, Villejuif, France.
Cell death and differentiation (Impact Factor: 8.18). 07/2011; 19(1):107-20. DOI: 10.1038/cdd.2011.96
Source: PubMed


In 2009, the Nomenclature Committee on Cell Death (NCCD) proposed a set of recommendations for the definition of distinct cell death morphologies and for the appropriate use of cell death-related terminology, including 'apoptosis', 'necrosis' and 'mitotic catastrophe'. In view of the substantial progress in the biochemical and genetic exploration of cell death, time has come to switch from morphological to molecular definitions of cell death modalities. Here we propose a functional classification of cell death subroutines that applies to both in vitro and in vivo settings and includes extrinsic apoptosis, caspase-dependent or -independent intrinsic apoptosis, regulated necrosis, autophagic cell death and mitotic catastrophe. Moreover, we discuss the utility of expressions indicating additional cell death modalities. On the basis of the new, revised NCCD classification, cell death subroutines are defined by a series of precise, measurable biochemical features.

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Available from: Lorenzo Galluzzi, Oct 13, 2015
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    • "The signaling pathways leading to RN exhibit a consistent degree of crosstalk with the molecular cascades that control and execute apoptosis [2] [23]. This functional interplay – which often occurs in the context of cell-wide responses to stress [152] – mainly reflects: (1) the existence of shared signal transducers, which can activate either apoptotic or necrotic cell death (e.g., TNFR1, AIF, p53), depending on the specific circumstances [19] [85] [94]; and (2) the existence of negative feedback circuitries whereby one cell death subroutine (most often apoptosis) actively inhibits the other (most frequently necrosis) (Figure 2) [153]. "
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    ABSTRACT: It is now clear that apoptosis does not constitute the sole genetically-encoded form of cell death. Rather, cells can spontaneously undertake or exogenously be driven into a cell death subroutine that manifests with necrotic features, yet can be inhibited by pharmacological and genetic interventions. As regulated necrosis (RN) plays a major role in both physiological scenarios (e.g., embryonic development) and pathological settings (e.g., ischemic disorders), consistent efforts have been made throughout the last decade toward the characterization of the molecular mechanisms that underlie this cell death modality. Contrarily to initial beliefs, RN does not invariably result from the activation of a receptor interacting protein kinase 3 (RIPK3)-dependent signaling pathway, but may be ignited by distinct molecular networks. Nowadays, various types of RN have been characterized, including (but not limited to) necroptosis, mitochondrial permeability transition (MPT)-dependent RN and parthanatos. Of note, the inhibition of only one of these modules generally exerts limited cytoprotective effects in vivo, underscoring the degree of interconnectivity that characterizes RN. Here, we review the signaling pathways, pathophysiological relevance and therapeutic implications of the major molecular cascades that underlie RN.
    Seminars in Cell and Developmental Biology 11/2014; 35. DOI:10.1016/j.semcdb.2014.02.006 · 6.27 Impact Factor
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    • "Programmed cell death is an evolutionary conserved pathway which governs the development and tissue homeostasis in multicellular organisms (Fuchs and Steller 2011; Jacobson et al. 1997). The Nomenclature Committee of Cell Death classified 13 types of cell death, but apoptosis, necrosis, and autophagy are the most commonly observed types of cell death in animals (Galluzzi et al. 2012). Despite the diversity in the molecular mechanisms of programmed cell death, most of them involve the contribution of key proteins, the caspases (Fuchs and Steller 2011). "
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    ABSTRACT: Fat body, typically comprising trophocytes, provides energy during metamorphosis. The fat body can be renewed once the larval phase is complete or recycled and relocated to form the fat body of the adult insect. This study aims to identify the class of programmed cell death that occurs within the fat body cells during the metamorphosis of the stingless bee Melipona quadrifasciata. Using immunodetection techniques, the fat body of the post-defecating larvae and the white-, pink-, brown-, and black-eyed pupae were tested for cleaved caspase-3 and DNA integrity, followed by ultrastructural analysis and identification of autophagy using RT-PCR for the Atg1 gene. The fat body of M. quadrifasciata showed some apoptotic cells positive for cleaved caspase-3, although without DNA fragmentation. During development, the fat body cells revealed an increased number of mitochondria and free ribosomes, in addition to higher amounts of autophagy Atg1 mRNA, than that of the pupae. The fat body of M. quadrifasciata showed few cells which underwent apoptosis, but there was evidence of increased autophagy at the completion of the larval stage. All together, these data show that some fat body cells persist during metamorphosis in the stingless bee M. quadrifasciata.
    Protoplasma 10/2014; 252(2). DOI:10.1007/s00709-014-0707-z · 2.65 Impact Factor
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    • "This aberrant mitosis may lead to apoptosis or necrosis (41). Of note, mitotic catastrophe is not considered a form of cell death, but rather an irreversible trigger for cell death (22). "
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    ABSTRACT: Histological tumor necrosis (TN) has been reported to indicate a poor prognosis for different human cancers. It is generally accepted that TN results from chronic ischemic injury due to rapid tumor growth. However, whether insufficient tumor vascularization and inadequate tumor cell oxygenation are the only factors causing TN remains controversial. Mitotic catastrophe is considered to occur as a result of dysregulated/failed mitosis, leading to cell death. We hypothesize that mitotic catastrophe, induced by hypoxic stress, may lead to the TN which is observed in high grade carcinomas. The current review describes the morphological features of TN in malignant epithelial tumors. In addition, evidence regarding the involvement of mitotic catastrophe in the induction of TN in human carcinomas is discussed.
    Oncology letters 10/2014; 8(4):1397-1402. DOI:10.3892/ol.2014.2345 · 1.55 Impact Factor
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