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Regulated cell death and adaptive stress responses
Open accessAbstract
Eukaryotic cells react to potentially dangerous perturbations of the intracellular or extracellular microenvironment by activating rapid (transcription-independent) mechanisms that attempt to restore homeostasis. If such perturbations persist, cells may still try to cope with stress by activating delayed and robust (transcription-dependent) adaptive systems, or they may actively engage in cellular suicide. This regulated form of cell death can manifest with various morphological, biochemical and immunological correlates, and constitutes an ultimate attempt of stressed cells to maintain organismal homeostasis. Here, we dissect the general organization of adaptive cellular responses to stress, their intimate connection with regulated cell death, and how the latter operates for the preservation of organismal homeostasis.
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“On the other hand, RCD can originate from perturbations of the intracellular or extracellular microenvironment, when such perturbations are too intense or prolonged for adaptative responses to cope with stress and restore cellular homeostasis [5].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [5]
In the citing paper
“However, while adaptative stress responses operate at the cellular level (which—by extension—promotes the maintenance of homeostasis at the level of organism or colony), RCD directly operates at the level of the organism or colony in spite of cellular homeostasis [5].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [5]
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“RCD relies on a dedicated molecular machinery, implying that it can be modulated (i.e., delayed or accelerated) by pharmacological or genetic interventions [5, 17].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [5]
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Metadata
- Authors
- Galluzzi, L., Bravo-San Pedro, J. M., Kepp, O., & Kroemer, G.
- Affiliations
- Inserm (FR)
- Karolinska University Hospital (SE)
- Corresponding author
- Galluzzi, Lorenzo
- Kroemer, Guido
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2016-04-05
- Volume
- 73
- Issue
- 11-12
- Pages
- 2405-2410
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11108439
- OpenAlex
- W2331898099
- Cited by
- 177
- References
- 53
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 26 · 2023: 26 · 2022: 18 · 2021: 16 · 2020: 17 · 2019: 13 · 2018: 23 · 2017: 11 · 2016: 5
- FWCI
- 1.57
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- regulated cell death, adaptive stress response, cellular homeostasis
- MeSH terms
- Autophagy, Eukaryotic Cells, Homeostasis, Mitochondria, Necrosis, Stress, Physiological, Signal Transduction, Apoptosis
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