ArticleJCI insight2020
Interaction between the autophagy protein Beclin 1 and Na+,K+-ATPase during starvation, exercise, and ischemia.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 52 citations in OpenAlex.
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- Oxidative Stress in the Regulation of Autosis-Related Proteins.Antioxidants (Basel, Switzerland) · 2025Review
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- Mitochondria as the central regulator of cell death in bronchopulmonary dysplasia.Frontiers in physiology · 2025Review
- A soluble garlic polysaccharide supplement alleviates fatigue in mice.NPJ science of food · 2024Article
- Neuronal autosis is NaCell death & disease · 2024Article
- Update on a brain-penetrant cardiac glycoside that can lower cellular prion protein levels in human and guinea pig paradigms.PloS one · 2024Article
- Insulin-like growth factor-1 reduces cardiac autosis through decreasing AMPK/FOXO1 signaling and NaArchives of medical science : AMS · 2024Article
- Autophagy: Regulator of cell death.Cell death & disease · 2023Review
- Moderate Hyperkalemia Regulates Autophagy to Reduce Cerebral Ischemia-Reperfusion Injury in a CA/CPR Rat Model.Brain sciences · 2023Article
- Acyl coenzyme A binding protein (ACBP): An aging- and disease-relevant "autophagy checkpoint".Aging cell · 2023Review
- An autophagy-inducing stapled peptide induces mitochondria dysfunction and triggers autotic cell death in triple-negative breast cancer.Cell death discovery · 2023Article
- Resveratrol promotes mitochondrial energy metabolism in exercise-induced fatigued rats.Nutrition research and practice · 2023Article
- Regulated cell death pathways in kidney disease.Nature reviews. Nephrology · 2023Review
- Review of machine perfusion studies in vascularized composite allotransplant preservation.Frontiers in transplantation · 2023Review
- The NaFrontiers in endocrinology · 2023Review
- Autosis as a selective type of cell death.Frontiers in cell and developmental biology · 2023Article
- LncRNAs and regulated cell death in tumor cells.Frontiers in oncology · 2023Review
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 4 countries.
Funding
Abstract
Autosis is a distinct form of cell death that requires both autophagy genes and the Na+,K+-ATPase pump. However, the relationship between the autophagy machinery and Na+,K+-ATPase is unknown. We explored the hypothesis that Na+,K+-ATPase interacts with the autophagy protein Beclin 1 during stress and autosis-inducing conditions. Starvation increased the Beclin 1/Na+,K+-ATPase interaction in cultured cells, and this was blocked by cardiac glycosides, inhibitors of Na+,K+-ATPase. Increases in Beclin 1/Na+,K+-ATPase interaction were also observed in tissues from starved mice, livers of patients with anorexia nervosa, brains of neonatal rats subjected to cerebral hypoxia-ischemia (HI), and kidneys of mice subjected to renal ischemia/reperfusion injury (IRI). Cardiac glycosides blocked the increased Beclin 1/Na+,K+-ATPase interaction during cerebral HI injury and renal IRI. In the mouse renal IRI model, cardiac glycosides reduced numbers of autotic cells in the kidney and improved clinical outcome. Moreover, blockade of endogenous cardiac glycosides increased Beclin 1/Na+,K+-ATPase interaction and autotic cell death in mouse hearts during exercise. Thus, Beclin 1/Na+,K+-ATPase interaction is increased in stress conditions, and cardiac glycosides decrease this interaction and autosis in both pathophysiological and physiological settings. This crosstalk between cellular machinery that generates and consumes energy during stress may represent a fundamental homeostatic mechanism.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.