Death by design: apoptosis, necrosis and autophagy.

By A. Edinger, Craig B. Thompson. Current Opinion in Cell Biology, 2004

1,484 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ea173952c1215e022a82ec3abb70b1f79a10dfa6

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Citations in the corpus

Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival (2008, background): “by commandeering pro-survival signalling pathways ( Box 3 ) and anti-apoptotic proteins (such as the anti-apoptotic BCL2 family members, Box 4 ) to suppress or neutralize death signal”
Subversion of Cellular Autophagosomal Machinery by RNA Viruses (2005, background): “The first possibility was that the RNAimediated reductions in the intracellular concentrations of Atg12p and LC3 protein reduced cell lysis and therefore lytic release of virus; links between autophagy and apoptosis have been reported (reviewed in [57,58]).”
Autophagy and signaling: their role in cell survival and cell death (2005, background): “panied by increased flux, can result in the death of cells that are not bioenergetically compromised would be a strong indication that autophagy is indeed a cell death mechanism in its own right, but this has yet to be demonstrated.(53) However, the fact that the molecular machinery of autophagy is ”
p53 opens the mitochondrial permeability transition pore to trigger necrosis (2012, background): “Three morphologically distinct types of cell death occur in physiologic and pathologic processes: apoptosis, autophagy, and necrosis (Edinger and Thompson, 2004).”
On the Mechanism of Cytoprotection by Ferrostatin-1 and Liproxstatin-1 and the Role of Lipid Peroxidation in Ferroptotic Cell Death (2017, neutral): “7,8 − 11 The induction of ferroptosis o ﬀ ers a new strategy for killing cancer cells, and disruption of the regulatory framework that keeps ferroptosis in check may contribute to the pathogenesis of degenerative diseases in which LOOH accumulation has been implicated.”
Staphylococcus aureus Leukocidin A/B (LukAB) Kills Human Monocytes via Host NLRP3 and ASC when Extracellular, but Not Intracellular (2015, background): “Traditionally, programmed cell death can be morphologically categorized into necrotic or apoptotic phenotypes [38,39].”
Regulation of Autophagy by Reactive Oxygen Species (ROS): Implications for Cancer Progression and Treatment (2009, positive): “Apoptosis is an orderly form of cell death that occurs through two major pathways, initiated either by death-receptor ligation (extrinsic pathway) or by release of apoptotic proteins from the mitochondria, including cytochrome c , Smac = Diablo, and Endo G (intrinsic pathway) (31).”
Molecular mechanisms of diabetic kidney disease. (2014, positive): “Inflammation is considered to be one of the critical pathways that can limit regeneration in adult mammalian organs (95).”
Bcl-2 family proteins and cancer (2008, background): “Prolonged nutrient deprivation invokes autophagy, an evolutionarily conserved response for catabolizing macromolecules and organelles, thereby generating substrates for ATP production (Edinger and Thompson, 2004; Lum et al., 2005).”