ArticleCells2018
A Rise in ATP, ROS, and Mitochondrial Content upon Glucose Withdrawal Correlates with a Dysregulated Mitochondria Turnover Mediated by the Activation of the Protein Deacetylase SIRT1.
Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 58 citations in OpenAlex.
- Bisphenol Z at environmentally relevant dose dysregulates mitochondrial metabolism and proliferative capacity in human ovarian granulosa cells by inducing changes in metabolic substrate utilization.Archives of toxicology · 2026Article
- Suramin Interactions Across Biological Systems: From Molecular Targets to Therapeutic Implications.Biomolecules · 2026Review
- Super-Resolution Imaging of Nuclear Pore Responses to Mechanical Stress and Energy Depletion.Viruses · 2026Article
- Dapagliflozin sustains heart function in type 3 cardiorenal syndrome by restoring DUSP1-dependent mitochondrial quality control.Acta diabetologica · 2026Article
- Article
- Ethanol Exposure Increases Oxygen Consumption by Developing Cerebral Arteries in a Trimester-, Concentration- and Sex-Dependent Manner.Biomolecules · 2025Article
- Profiling the effect of low frequency mechanical vibration on the metabolic and oxidative stress responses of A431 carcinoma.FEBS open bio · 2025Article
- Mito-TEMPO Mitigates Fibromyalgia Induced by Reserpine in Rats: Orchestration Between SIRT1, Mitochondrial Dynamics, Endoplasmic Reticulum and miRNA-320.Neurochemical research · 2025Article
- Potential effects of adenosine triphosphate and melatonin on oxidative and inflammatory optic nerve damage in rats caused by 5-fluorouracil.International journal of ophthalmology · 2025Article
- Blast-Overpressure Induced Modulation of PARP-SIRT-NRF2 Axis in Stress Signaling of Astrocytes and Microglia.Immunity, inflammation and disease · 2025Article
- Impaired Autophagic Flux in Glucose-Deprived Cells: An Outcome of Lysosomal Acidification Failure Exacerbated by Mitophagy Dysfunction.Molecules and cells · 2023Review
- Multifaceted roles of mitochondrial dysfunction in diseases: from powerhouses to saboteurs.Archives of pharmacal research · 2023Review
- SIRT1 activation promotes energy homeostasis and reprograms liver cancer metabolism.Journal of translational medicine · 2023Article
- Examining Sporadic Cancer Mutations Uncovers a Set of Genes Involved in Mitochondrial Maintenance.Genes · 2023Article
- The αMSH-Dependent PI3K Pathway Supports Energy Metabolism, via Glucose Uptake, in Melanoma Cells.Cells · 2023Article
- AMPK-induced mitochondrial biogenesis decelerates retinal pigment epithelial cell degeneration under nutrient starvation.BMB reports · 2023Article
- Highly concentrated trehalose induces prohealing senescence-like state in fibroblasts via CDKN1A/p21.Communications biology · 2023Article
- Adipose stromal vascular fraction reverses mitochondrial dysfunction and hyperfission in aging-induced coronary microvascular disease.American journal of physiology. Heart and circulatory physiology · 2022Article
- The potential inhibitory effect of ginsenoside Rh2 on mitophagy in UV-irradiated human dermal fibroblasts.Journal of ginseng research · 2022Article
- Therapeutic Potential of Mitophagy-Inducing Microflora Metabolite, Urolithin A for Alzheimer's Disease.Nutrients · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose withdrawal has been used as a model for the study of homeostatic defense mechanisms, especially for how cells cope with a shortage of nutrient supply by enhancing catabolism. However, detailed cellular responses to glucose withdrawal have been poorly studied, and are controversial. In this study, we determined how glucose withdrawal affects mitochondrial activity, and the quantity and the role of SIRT1 in these changes. The results of our study indicate a substantial increase in ATP production from mitochondria, through an elevation of mitochondrial biogenesis, mediated by SIRT1 activation that is driven by increased NAD⁺/NADH ratio. Moreover, mitochondria persisted in the cells as elongated forms, and apparently evaded mitophagic removal. This led to a steady increase in mitochondria content and the reactive oxygen species (ROS) generated from them, indicating failure in ATP and ROS homeostasis, due to a misbalance in SIRT1-mediated mitochondria turnover in conditions of glucose withdrawal. Our results suggest that SIRT1 activation alone cannot properly manage energy homeostasis under certain metabolic crisis conditions.
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Registered trials
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 OpenQuestion graph.