Autosis is a Na + ,K + -ATPase–regulated form of cell death triggered by autophagy-inducing peptides, starvation, and hypoxia–ischemia
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Significance: We show that the selective overactivation of autophagy can cause cell death with unique morphological features distinct from apoptosis or necrosis. This unique type of autophagic cell death, termed “autosis,” occurs not only in vitro but also in vivo in cerebral hypoxia–ischemia. Moreover, autosis is inhibited both in vitro and in vivo by cardiac glycosides, which are Na + ,K + -ATPase antagonists used in clinical medicine. Our findings contribute to the basic understanding of cell-death mechanisms and suggest strategies for protecting cells against stresses such as hypoxia–ischemia.
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Na+/K+-ATPase inhibitors such as cardiac glycosides confer neuroprotection in a rat model of neonatal hypoxia-ischemia.
“Corroborating the physiological relevance of this process, the administration of Na+/K+-ATPase inhibitors such as cardiac glycosides, confers neuroprotection in a rat model of neonatal hypoxia-ischemia [851].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [851]
Autosis relies on plasma membrane Na+/K+-ATPase.
“Autosis is a specific variant of autophagy-dependent cell death that relies on the plasma membrane Na+/K+-ATPase [851].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [851]
RCD is a primary etiological determinant in diseases with irreversible loss of post-mitotic tissues such as myocardial infarction and neurodegeneration.
“On the one hand, RCD constitutes a primary etiological determinant in diseases associated with the irreversible loss of post-mitotic tissues (e.g., myocardial infarction, neurodegeneration) [687, 752, 851, 869, 1035, 1036].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [851]
Glucocorticoid reduced the autophagic gene expression including key genes associated with autophagy induction, such as Atg7 and Beclin 1, by 1-5 folds.
“We found that GC reduced the autophagic gene expression including key genes associated with autophagy induction, such as Atg7 and Beclin 1[45], by 1-5 folds”
From Prevention of glucocorticoid induced bone changes with beta-ecdysone (2015) · cites this paper as [45]
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“The Tat-Beclin 1 peptide complex may initiate autosis, with the fusion of the evolutionarily conserved, 18-amino acid-long Beclin 1 domain with 11 amino acids from the HIV Tat protein transduction domain aiding the cellular entry of the fusion peptide [169] .”
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“In most cases, autophagy promotes cell survival, but as with certain environments, particularly cancer cell death induced by lower organisms or drugs [119, 120], autophagy may actually induce cell death in a process known as autophagy-dependent cell death (ACDC) or autosis [120, 121, 122].”
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InfluentialAutophagy protein ATG16L1 prevents necroptosis in the intestinal epithelium
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BackgroundNeuronal Death Mechanisms and Therapeutic Strategy in Ischemic Stroke
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“Moreover, selective overexpression of autophagy can cause a special type of regulated cell death termed " autosis, " which is mediated by the Na + , K + -ATPase pump (Liu et al., 2013).”
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BackgroundRegulation of autophagy by Beclin 1 in the heart
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InfluentialAutophagy in acute brain injury
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Guidelines for evaluating myocardial cell death
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BackgroundChloroquine and hydroxychloroquine for cancer therapy
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“, 2012]) and autophagic cell death are now known to contribute to cell death induced by viral infection (Linkermann and Green, 2014) and nutrient deprivation (Gao et al., 2015; Liu et al., 2013) and to programmed cell death during development (Nelson et al.”
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STING orchestrates the neuronal inflammatory stress response in multiple sclerosis
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“This form of cell death coincides well with autosis, a recently characterized Na,K-ATPase-regulated form of cell death [36].”
BackgroundInfluentialMyocardial stress and autophagy: mechanisms and potential therapies
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“For example, autosis is a specific form of ADCD that involves the Na/K-ATPase [139].”
BackgroundRecent insights into cell death and autophagy
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Repair, Reuse, Recycle: The Expanding Role of Autophagy in Genome Maintenance
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Autophagy in Cell Life and Cell Death
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BackgroundCell Death in the Developing Brain after Hypoxia-Ischemia
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BackgroundInfluentialNeuroprotection by selective neuronal deletion of <i>Atg7</i> in neonatal brain injury
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“Autosis is a subtype of ADCD that relies on the plasma membrane Na + /K + -ATPase [43].”
BackgroundUpregulation of Rubicon promotes autosis during myocardial ischemia/reperfusion injury
Nah, J., Zhai, P., Huang, C.-Y., Fernández, Á. F., Mareedu, S., Levine, B., & Sadoshima, J. (2020) · Journal of Clinical Investigation · doi:10.1172/jci132366 · Cited by 150 · see citing works
“Levine and colleagues showed that autosis is induced by hypoxia-ischemia in the neonatal mouse brain in vivo (11); howAlthough autophagy is generally protective, uncontrolled or excessive activation of autophagy can be detrimental.”
BackgroundInfluentialSelf-citationDiversity-Oriented Stapling Yields Intrinsically Cell-Penetrant Inducers of Autophagy
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Self-citationA compendium of kinetic modulatory profiles identifies ferroptosis regulators
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“Cultured cells that are starved or exposed to a Beclin1-derived peptide, neurons in cerebral ischemia, and hepatocytes of patients with severe anorexia nervosa exhibit hallmarks of autosis (Kheloufi et al. 2015, Liu et al. 2013, C. Xie et al. 2016).”
BackgroundAutophagy in neurodegeneration: New insights underpinning therapy for neurological diseases
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“In 2013, a study was published demonstrating that selective over-activation of autophagy could cause a pattern of cell death with morphological characteristics different from apoptosis or necrosis, termed “autosis” (Liu et al. 2013) (Table 1).”
BackgroundSelf‐Assembled Autophagy‐Inducing Polymeric Nanoparticles for Breast Cancer Interference In‐Vivo
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Regorafenib induces lethal autophagy arrest by stabilizing PSAT1 in glioblastoma
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“Besides apoptosis, pathways that promote cell death include: autophagy-associated cell death [17], autosis [18], paraptosis [19], entosis [20], ferroptosis [21] and programmed necrosis [22], all of which can contribute to tumor inhibition.”
Programmed Cell Death and Inflammation: Winter Is Coming
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“Morphologically, autosis is characterized by numerous autophagosomes, plasma membrane rupture, enhanced cell substrate adhesion, focal ballooning of perinuclear space, and disruption of endoplasmic reticulum [59].”
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Ceramide induced mitophagy and tumor suppression
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- Authors
- Liu, Y., Shoji-Kawata, S., Sumpter, R. M., Wei, Y., Ginet, V., Zhang, L., Posner, B., Tran, K. A., Green, D. R., Xavier, R. J., Shaw, S. Y., Clarke, P. G. H., Puyal, J., & Levine, B.
- Affiliations
- Center for Autophagy Research,
- Howard Hughes Medical Institute (US)
- University of Lausanne (CH)
- Biochemistry, and
- Center for Systems Biology (US)
- St. Jude Children's Research Hospital (US)
- Broad Institute (US)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2013-11-25
- Volume
- 110
- Issue
- 51
- Pages
- 20364-20371
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3870705
- OpenAlex
- W2145084709
- Cited by
- 607
- References
- 35
- Citations by year
- 2026: 33 · 2025: 48 · 2024: 38 · 2023: 51 · 2022: 46 · 2021: 58 · 2020: 50 · 2019: 51 · 2018: 43 · 2017: 58 · 2016: 47 · 2015: 43 · 2014: 38
- FWCI
- 31.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (acceptedVersion, other-oa)
- IRIS (submittedVersion)
- Funders
- National Science Foundation (310030)
- Howard Hughes Medical Institute
- McKnight Foundation
- University of Texas Southwestern Medical Center
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (130769, 310030)
- Université de Lausanne
- National Institutes of Health (HHSN268201000044C, 5p01ca095471-10, 1P01CA95471-09)
- U.S. Public Health Service (R01 A140646)
- National Heart, Lung, and Blood Institute (HHSN268201000044C)
- National Cancer Institute (P01 CA95471, P01-CA095471, R01CA169291, CA109618, HHSN268201000044C, (CA142543), R01CA109618, P30CA142543)
- National Institute of Allergy and Infectious Diseases (R01AI040646, U54AI057156)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- autophagic cell death, Na+/K+-ATPase, Beclin-1, starvation, hypoxia-ischemia, hippocampal neurons, cardiac glycosides, Na+/K+-ATPase alpha1 subunit, autophagosomes, cell death regulation
- MeSH terms
- Sodium-Potassium-Exchanging ATPase, Animals, Autophagy, Cardiac Glycosides, Brain Ischemia, HeLa Cells, Humans, Nerve Tissue Proteins, Rats, Cell-Penetrating Peptides
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