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Autosis is a Na + ,K + -ATPase–regulated form of cell death triggered by autophagy-inducing peptides, starvation, and hypoxia–ischemia
Open accessAbstract
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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“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]
In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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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“Autosis, a form of autophagy-dependent cell death, opens the Na + /K + -ATPase signaling (Liu et al. 2013).”
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Féraille, E., & Eladari, D. (2026) · Elsevier eBooks · doi:10.1016/b978-0-12-815389-5.00056-3
Multilayered molecular architecture orchestrating programmed cell death in mucosal barriers tissues
Liu, T., Zhang, Q., Chen, D., Chen, Y., Al-Azab, M., Shaher, F., Zhang, Y., Chen, R., & Zhou, A. X. (2026) · Oral Science and Homeostatic Medicine · doi:10.26599/oshm.2026.9610051
Dual regulation of autophagy: paradoxical effects on tumor angiogenesis
Xiang, S., Gong, X., Zhou, J., Qiu, T., Lan, Y., Zhang, Z., & Ji, Y. (2026) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2026.1872152
“…fragmentation (early stage), and ER depletion and disappearance (late stage), as well as nuclear envelope invagination (early stage) and localized swelling of the perinuclear space (late stage) (Liu and Levine, 2015), as well as a unique dependence on the sodium-potassium ATPase (Liu et al., 2013).”
Repurposing Antipsychotics in Cancer Therapy: Modulation of Autophagy Mechanisms
Sarkani, E. O., Parsa, S., Darash, S., Chaleshtori, Z. M., Taghizadeh, M., Yahyazadeh, S., & Vakili, O. (2026) · Clinical Drug Investigation · doi:10.1007/s40261-026-01579-3
“Cell death is mediated by the Na + /K + ATPase pump and is associated with the irregular accumulation of autophagosomes [102].”
Lakshmanan, D. K., Thilagar, S., Shanmugam, A., Kalidass, B., & Ravichandran, G. (2026) · Tissue and Cell · doi:10.1016/j.tice.2026.103767
Autosis: The known and the unknown
Piedra-Macías, A., Guerra‐Andrés, M., & Fernández, Á. F. (2026) · International review of cytology · doi:10.1016/bs.ircmb.2026.07.004
Metadata
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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