Autophagy and the integrated stress response

By Guido Kroemer, Guillermo Mariño, Beth Levine. Molecules and Cells, 2010

3,412 citations recorded by the source corpus.

Autophagy is a tightly regulated pathway involving the lysosomal degradation of cytoplasmic organelles or cytosolic components. This pathway can be stimulated by multiple forms of cellular stress, including nutrient or growth factor deprivation, hypoxia, reactive oxygen species, DNA damage, protein aggregates, damaged organelles or intracellular pathogens. Both specific, stimulus-dependent and more general stimulus-independent signaling pathways are activated to coordinate different phases of autophagy. Autophagy can be integrated with other cellular stress responses through parallel stimulation of autophagy and other stress responses by specific stress stimuli, through dual regulation of autophagy and other stress responses by multi-functional stress signaling molecules, and/or through mutual control of autophagy and other stress responses. Thus, autophagy is a cell biological process that is a central component of the integrated stress response.

Subfields: Epidemiology, Pharmacology, Plant Science

View Paper: https://www.semanticscholar.org/paper/f34e5e528789cc38a84c81ae43d4a8d093daaabe

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Citations in the corpus

The unfolded protein response: controlling cell fate decisions under ER stress and beyond (2012, background): “Macroautophagy, a bulk degradation pathway, is also activated by ER stress, possibly to eliminate damaged ER (a process termed ER-phagy) and abnormal protein aggregates through the lysosomal pathwa”
Mammalian MAPK signal transduction pathways activated by stress and inflammation: a 10-year update. (2012, background): “Autophagy also coincides with the proteasomal degradation of sequestome-1 (p62/SQSTM1) which binds autophagic target proteins and LC3-II (160, 174, 342) (FIGURE 7).”
MicroRNA Functions in Stress Responses (2010, neutral): “, 2010), rapid clearance of damaged macromolecules (Kroemer et al., 2010), growth arrest, activation of certain gene expression programs (Spriggs et al.”
The integrated stress response (2016, neutral): “However, it has been suggested that mechanisms directed from eIF2 a phosphorylation other than selective translation of ATF4 mRNA might also be involved in the activation of autophagy [170].”
Autophagy promotes ferroptosis by degradation of ferritin (2016, background): “In many cases, induction of autophagy promotes cell survival in response to environmental stressors such as nutritional starvation and energy depletion.(2) In some cases, excessive and impaired autophagy may contribute to cell death.”
Autophagy-Dependent Ferroptosis: Machinery and Regulation (2020, background): “Thus, autophagy is generally beneficial for cellular survival in response to environmental stresses ranging from nutrient starvation to growth factor depletion, hypoxia, temperature change, and infectious pathogens (Kroemer et al., 2010; Murrow and Debnath, 2013).”
Autophagy‐based unconventional secretory pathway for extracellular delivery of IL‐1β (2011, background): “For the most part, autophagy enables cellular viability (Kroemer and Levine, 2008; Kroemer et al, 2010) by removing damaged organelles, for example, depolarized or leaky mitochondria (Youle and Narendra, 2011), digesting potentially toxic protein aggregates (Renna et al, 2010),…”
Molecular mechanisms of cisplatin resistance (2012, background): “Kroemer et al., 2010; Ren et al., 2010; Yu et al., 2011 DYRK1B Conserved kinase that mediates differentiation in multiple tissues.”