ArticleStem cells (Dayton, Ohio)2016
SCO2 Mediates Oxidative Stress-Induced Glycolysis to Oxidative Phosphorylation Switch in Hematopoietic Stem Cells.
Article in Stem cells (Dayton, Ohio), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Effects of cuproptosis and its application in inflammatory bowel disease (Review).International journal of molecular medicine · 2026Review
- Mapping malignant T-cell states and immune circuits in Sézary syndrome by single-cell analysis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026Article
- Platelets facilitate fat grafting by mitochondrial transfer and reducing oxidative stress in adipose-derived stem cells.Stem cells translational medicine · 2025Article
- Targeting bone marrow mesenchymal stromal cell-derived IL-6 to overcome acute myeloid leukemia chemoresistance.Blood advances · 2025Observational
- Metabolic Signature ofJournal of personalized medicine · 2025Review
- Exploring the Functionality of the Krüppel-like Factors in Kidney Development, Metabolism, and Diseases.Life (Basel, Switzerland) · 2024Review
- Protective effect of fructooligosaccharide against oxidative stress and apoptosis induced by Aeromonas hydrophila in Megalobrama amblycephala.BMC genomics · 2024Article
- Crosstalk between DNA Damage Repair and Metabolic Regulation in Hematopoietic Stem Cells.Cells · 2024Review
- Disruption of mitochondrial energy metabolism is a putative pathogenesis of Diamond-Blackfan anemia.iScience · 2024Article
- Oxygen and Iron Availability Shapes Metabolic Adaptations of Cancer Cells.World journal of oncology · 2024Review
- The implications and prospect of cuproptosis-related genes and copper transporters in cancer progression.Frontiers in oncology · 2023Review
- Single-Cell RNA Transcriptomics Reveals the State of Hepatic Lymphatic Endothelial Cells in Hepatitis B Virus-Related Acute-on-Chronic Liver Failure.Journal of clinical medicine · 2022Article
- Exploring the Metabolic Landscape of AML: From Haematopoietic Stem Cells to Myeloblasts and Leukaemic Stem Cells.Frontiers in oncology · 2022Review
- Genome-wide whole-blood transcriptome profiling across inherited bone marrow failure subtypes.Blood advances · 2021Article
- Understanding cell culture dynamics: a tool for defining protocol parameters for improved processes and efficient manufacturing using human embryonic stem cells.Bioengineered · 2021Article
- FANCD2 and HES1 suppress inflammation-induced PPARɣ to prevent haematopoietic stem cell exhaustion.British journal of haematology · 2021Article
- Mitochondria in cancer.Cell stress · 2020Review
- Fancd2-deficient hematopoietic stem and progenitor cells depend on augmented mitochondrial translation for survival and proliferation.Stem cell research · 2019Article
- p53-TP53-Induced Glycolysis Regulator Mediated Glycolytic Suppression Attenuates DNA Damage and Genomic Instability in Fanconi Anemia Hematopoietic Stem Cells.Stem cells (Dayton, Ohio) · 2019Article
- An evolutionary perspective on immunometabolism.Science (New York, N.Y.) · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Fanconi anemia (FA) is an inherited bone marrow (BM) failure syndrome, presumably resulting from defects in hematopoietic stem cells (HSCs). Normal HSCs depend more on glycolysis than on oxidative phosphorylation (OXPHOS) for energy production. Here, we show that FA HSCs are more sensitive to the respiration inhibitor NaN3 treatment than to glycolytic inhibitor 2-deoxy-d-glucose (2-DG), indicating more dependence on OXPHOS. FA HSCs undergo glycolysis-to-OXPHOS switch in response to oxidative stress through a p53-dependent mechanism. Metabolic stresses induce upregulation of p53 metabolic targets in FA HSCs. Inactivation of p53 in FA HSCs prevents glycolysis-to-OXPHOS switch. Furthermore, p53-deficient FA HSCs are more sensitive to 2-DG-mediated metabolic stress. Finally, oxidative stress-induced glycolysis-to-OXPHOS switch is mediated by synthesis of cytochrome c oxidase 2 (SCO2). These findings demonstrate p53-mediated OXPHOS function as a compensatory alteration in FA HSCs to ensure a functional but mildly impaired energy metabolism and suggest a cautious approach to manipulating p53 signaling in FA.
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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.