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Autophagy and the Integrated Stress Response
Open accessAbstract
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 multifunctional 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.
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“macro-autophagy (hereafter referred to as autophagy)—a tightly regulated major lysosomal degradation pathway (27–30)—has been implicated in establishing the SASP through the target of rapamycin (TOR) autophagy spatial coupling compartment (TASCC).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [28]
In the citing paper
“The array of MTOR-independent methods for stimulating autophagy also includes direct stimulation of AKT and BECN1, activating MAPK8/JNK1 to dissociate BCL2 from (and thereby disinhibit) BECN1, applying the synthetic peptide Tat-Beclin 1, SIRT1-associated starvation, and disrupting nonsense-mediated RNA decay [513–517] (Figure 3).”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [513]
In the citing paper
“Intracellular stress, which can be induced by reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, hypoxia, DNA damage and immune signalling, has also been demonstrated as a potential stimulator of autophagy”
From Autophagy in kidney homeostasis and disease (2020) · cites this paper as [14]
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Metadata
- Authors
- Kroemer, G., Mariño, G., & Levine, B.
- Affiliations
- Inserm (FR)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Kroemer, Guido
- Levine, Beth
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2010-10
- Volume
- 40
- Issue
- 2
- Pages
- 280-293
- ISSN
- 1097-2765 (ISSN-L)
- PMC
- PMC3127250
- OpenAlex
- W2157096314
- Cited by
- 3,506
- References
- 103
- Citations by year
- 2026: 100 · 2025: 163 · 2024: 177 · 2023: 193 · 2022: 245 · 2021: 291 · 2020: 269 · 2019: 251 · 2018: 264 · 2017: 281 · 2016: 258 · 2015: 255 · 2014: 254 · 2013: 210 · 2012: 181
- FWCI
- 18.11
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Consultation of the Doctoral Thesis Database (TESEO) (Ministerio de Educación, Cultura y Deporte) (submittedVersion, cc-by-nc-nd)
- Funders
- Howard Hughes Medical Institute
- National Cancer Institute (R01CA109618, R01CA084254)
- National Institute of Allergy and Infectious Diseases (R01AI051367)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- autophagy, integrated stress response, cellular stress response, lysosomal degradation, nutrient deprivation, hypoxia, reactive oxygen species, DNA damage, protein aggregates, intracellular pathogens, stress signaling pathways, organelle degradation
- MeSH terms
- Animals, Autophagy, Humans, Lysosomes, Models, Biological, Stress, Physiological, Signal Transduction, Cellular Senescence, Apoptosis, Cell Proliferation
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