Self-eating and self-killing: crosstalk between autophagy and apoptosis

By M. Maiuri, Einat Zalckvar, Adi Kimchi, Guido Kroemer. Nature reviews. Molecular cell biology, 2007

3,587 citations recorded by the source corpus.

Subfields: Cell Biology, Epidemiology, Geriatrics and Gerontology

View Paper: https://www.semanticscholar.org/paper/caf1104a254de6ab0e3f3f073d260a85fe1c6c84

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Citations in the corpus

Chondrocyte Apoptosis in the Pathogenesis of Osteoarthritis (2015, background): “Autophagy has been shown to engage in a complex cross-talk with apoptosis, initiated by shared upstream signals, sometimes resulting in simultaneous autophagy and apoptosis [102].”
Regulation of Autophagy by Reactive Oxygen Species (ROS): Implications for Cancer Progression and Treatment (2009, positive): “Autophagic cell death or ‘‘programmed cell death type two’’ (PCD II) is characterized by morphologic and molecular features that are distinct from apoptosis (PCD I) (74).”
Lysosomal membrane permeabilization in cell death (2008, background): “…was initially described as a type of cellular demise, it remains unclear whether autophagy represents an independent mode of programmed cell death, a backup mechanism of cell death when apoptosis is inhibited or simply a stress response that is activated in damaged cells (Maiuri et al., 2007).”
Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology. (2010, background): “generally accepted in some fields [73] but alternative interpretations have been proposed [74].”
Mitochondrial fusion, fission and autophagy as a quality control axis: the bioenergetic view. (2008, background): “While autophagy is commonly considered involved in cell death pathways [9], it has a number of other functions required for cellular adaptation.”
Autophagy: a lysosomal degradation pathway with a central role in health and disease. (2009, background): “Autophagy can benefit the progression of the tumor because it canprovide nutrients during starvation [129,130,138].”
Loss of autophagy diminishes pancreatic beta cell mass and function with resultant hyperglycemia. (2008, background): “…presumably through a direct effect on mitochondria, or deinhibit the activa- tion of caspases or permeabilization of mitochondrial outer membrane (Maiuri et al., 2007). p27 activated by metabolic stress and energy deficiency may also lead to cell-cycle arrest and decreased proliferation (Liang…”
Caspase-mediated cleavage of Beclin-1 inactivates Beclin-1-induced autophagy and enhances apoptosis by promoting the release of proapoptotic factors from mitochondria (2010, background): “Stressinduced autophagy is a mechanism that, depending on cell type and stimulus, either promotes or counteracts cell death.(22) Under conditions of growth factor starvation, when cellular self-maintenance is impeded, autophagy breaks down unnecessary proteins and damaged organelles to recycle metab”
Anti-apoptosis and cell survival: a review. (2011, background): “For example, autophagic like PCD occurs in response to apoptotic stimuli in cells that are unable to carry out apoptosis due to pharmacological inhibition or due to specific gene knockouts (double Bak and Bax KOs) [25,342,377].”
Hypoxia and cancer (2007, background): “Macroautophagy is a process that allows cells to recycle intracellular organelles such as ribosomes and mitochondria for nutritional and protective purposes [25].”