Autophagic cell death exists

Clarke, Peter G. H.; Puyal, Julien

doi:10.4161/auto.20380

Cited by 107 publications

(72 citation statements)

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“…Autophagy is a highly conserved process occurring in physiological conditions and stimulated under different types of stress including nutritional stress, as a mechanism to provide energy and sustain cell survival [20][21][22]. However, excessive autophagic digestion can lead to cell death [23,24]. Autophagy is initiated by the formation of a multiprotein complex containing Beclin 1 and class III PI3K, which are essential for the formation of double membrane vesicles or autophagosomes.…”

Section: Introductionmentioning

confidence: 99%

The Ketone Body, β-Hydroxybutyrate Stimulates the Autophagic Flux and Prevents Neuronal Death Induced by Glucose Deprivation in Cortical Cultured Neurons

et al. 2015

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Glucose is the major energy substrate in brain, however, during ketogenesis induced by starvation or prolonged hypoglycemia, the ketone bodies (KB), acetoacetate and β-hydroxybutyrate (BHB) can substitute for glucose. KB improve neuronal survival in diverse injury models, but the mechanisms by which KB prevent neuronal damage are still not well understood. In the present study we have investigated whether protection by the D isomer of BHB (D-BHB) against neuronal death induced by glucose deprivation (GD), is related to autophagy. Autophagy is a lysosomal-dependent degradation process activated during nutritional stress, which leads to the digestion of damaged proteins and organelles providing energy for cell survival. Results show that autophagy is activated in cortical cultured neurons during GD, as indicated by the increase in the levels of the lipidated form of the microtubule associated protein light chain 3 (LC3-II), and the number of autophagic vesicles. At early phases of glucose reintroduction (GR), the levels of p62 declined suggesting that the degradation of the autophagolysosomal content takes place at this time. In cultures exposed to GD and GR in the presence of D-BHB, the levels of LC3-II and p62 rapidly declined and remained low during GR, suggesting that the KB stimulates the autophagic flux preventing autophagosome accumulation and improving neuronal survival.

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Section: Introductionmentioning

confidence: 99%

The Ketone Body, β-Hydroxybutyrate Stimulates the Autophagic Flux and Prevents Neuronal Death Induced by Glucose Deprivation in Cortical Cultured Neurons

et al. 2015

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“…However, in other situations, autophagy can be deleterious and contribute to cell death either by triggering apoptosis or necrosis or as an independent cell death mechanism ("autophagic cell death" or type II programmed cell death). 2,3 In neurons the question of whether enhanced autophagy promotes cell death or cell survival is a subject of considerable debate [3][4][5][6][7][8] especially in excitotoxic conditions such as cerebral ischemia. Some studies have suggested a protective role of neuronal autophagy in cerebral hypoxia/ ischemia, 9,10 whereas others have demonstrated a death-mediating role.…”

Section: Introductionmentioning

confidence: 99%

Involvement of autophagy in hypoxic-excitotoxic neuronal death

et al. 2014

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“…[4][5][6] Conversely, recent reports have shown that excessive autophagic activities causing overconsumption of critical cellular components are responsible for type II nonapoptotic programmed cell death (also known as autophagic cell death). 5,[7][8][9] The complex functional mechanisms underlying the dual effects of autophagy are yet to be completely elucidated, and remain a current focus of research.…”

Section: Introductionmentioning

confidence: 99%