Cited by 239Cell death mechanisms and regulationAutophagy in Disease and TherapyMitochondrial Function and Pathology

Organelle-specific initiation of cell death

Galluzzi, Lorenzo, Bravo-San Pedro, José Manuel, Kroemer, Guido·2014·Nature Cell Biology

Abstract

In a majority of pathophysiological settings, cell death is not accidental - it is controlled by a complex molecular apparatus. Such a system operates like a computer: it receives several inputs that inform on the current state of the cell and the extracellular microenvironment, integrates them and generates an output. Thus, depending on a network of signals generated at specific subcellular sites, cells can respond to stress by attemptinwg to recover homeostasis or by activating molecular cascades that lead to cell death by apoptosis or necrosis. Here, we discuss the mechanisms whereby cellular compartments - including the nucleus, mitochondria, plasma membrane, endoplasmic reticulum, Golgi apparatus, lysosomes, cytoskeleton and cytosol - sense homeostatic perturbations and translate them into a cell-death-initiating signal.

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Crossref · 10.1038/ncb3005

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  • Pro-apoptotic BH3-only proteins are activated transcriptionally or post-translationally as specific organelles or cellular compartments experience perturbations of homeostasis, operating as cellular transducers of stress signaling.

    “These pro-apoptotic members of the BCL2 protein family (which contain a single BH3 domain) are activated transcriptionally or post-translationally as specific organelles or cellular compartments experience perturbations of homeostasis, de facto operating as cellular transducers of stress signaling [60–63].”

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Authors
Galluzzi, L., Bravo-San Pedro, J. M., & Kroemer, G.
Affiliations
  • Sorbonne Paris Cité (FR)
  • Inserm (FR)
Corresponding author
  • Galluzzi, Lorenzo
  • Kroemer, Guido
Venue
Nature Cell Biology
Published
2014-08
Volume
16
Issue
8
Pages
728-736
ISSN
  • 1465-7392 (ISSN-L)
  • 1476-4679
OpenAlex
W2036020241
Cited by
239
References
151
Citations by year
2026: 7 · 2025: 8 · 2024: 9 · 2023: 11 · 2022: 13 · 2021: 20 · 2020: 20 · 2019: 15 · 2018: 28 · 2017: 21 · 2016: 36 · 2015: 39 · 2014: 10 · 2013: 1
FWCI
3.33
Type
journal article
Language
en
Open access
closed
Locations
  • Nature Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Ligue Contre le Cancer
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
cell death, apoptosis, necrosis, mitochondrial signaling, endoplasmic reticulum stress, lysosomes, Golgi apparatus, cytoskeleton, plasma membrane, nuclear signaling, subcellular signaling
MeSH terms
Cell Membrane, Cell Nucleus, Cytoskeleton, Endoplasmic Reticulum, Golgi Apparatus, Humans, Lysosomes, Mitochondria, Models, Biological, Necrosis, Stress, Physiological, Organelles, Signal Transduction, Cell Death, Apoptosis

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