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hal.structure.identifierInstitut de Génétique Moléculaire de Montpellier [IGMM]
dc.contributor.authorOBUROGLU, L.
hal.structure.identifierInstitut de Mécanique et d'Ingénierie de Bordeaux [I2M]
dc.contributor.authorROMANO, M.
hal.structure.identifierInstitut de Génétique Moléculaire de Montpellier [IGMM]
dc.contributor.authorTAYLOR, N.
hal.structure.identifierInstitut de Génétique Moléculaire de Montpellier [IGMM]
dc.contributor.authorKINET, S.
dc.date.accessioned2021-05-14T09:41:49Z
dc.date.available2021-05-14T09:41:49Z
dc.date.issued2016
dc.identifier.issn1065-6251
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/76672
dc.description.abstractEnPURPOSE OF REVIEW: Hematopoietic stem cell (HSC) renewal and lineage differentiation are finely tuned processes, regulated by cytokines, transcription factors and cell-cell contacts. However, recent studies have shown that fuel utilization also conditions HSC fate. This review focuses on our current understanding of the metabolic pathways that govern HSC self-renewal, commitment and specification to the erythroid lineage. RECENT FINDINGS: HSCs reside in a hypoxic bone marrow niche that favors anaerobic glycolysis. Although this metabolic pathway is required for stem cell maintenance, other pathways also play critical roles. Fatty acid oxidation preserves HSC self-renewal by promoting asymmetric division, whereas oxidative phosphorylation induces lineage commitment. Committed erythroid progenitors support the production of 2.4 million erythrocytes per second in human adults via a synchronized regulation of iron, amino acid and glucose metabolism. Iron is indispensable for heme biosynthesis in erythroblasts; a process finely coordinated by at least two hormones, hepcidin and erythroferrone, together with multiple cell surface iron transporters. Furthermore, hemoglobin production is promoted by amino acid-induced mTOR signaling. Erythropoiesis is also strictly dependent on glutamine metabolism; under conditions where glutaminolysis is inhibited, erythropoietin-signaled progenitors are diverted to a myelomonocytic fate. Indeed, the utilization of both glutamine and glucose in de-novo nucleotide biosynthesis is a sine qua non for erythroid differentiation. SUMMARY: Diverse metabolic networks function in concert with transcriptional, translational and epigenetic programs to regulate HSC potential and orient physiological as well as pathological erythroid differentiation.
dc.language.isoen
dc.publisherLippincott, Williams & Wilkins
dc.title.enMetabolic regulation of hematopoietic stem cell commitment and erythroid differentiation
dc.typeArticle de revue
dc.identifier.doi10.1097/MOH.0000000000000234
dc.subject.halSciences du Vivant [q-bio]/Biochimie, Biologie Moléculaire
bordeaux.journalCurrent Opinion in Hematology
bordeaux.page198--205
bordeaux.volume23
bordeaux.hal.laboratoriesInstitut de Mécanique et d’Ingénierie de Bordeaux (I2M) - UMR 5295*
bordeaux.issue3
bordeaux.institutionUniversité de Bordeaux
bordeaux.institutionBordeaux INP
bordeaux.institutionCNRS
bordeaux.institutionINRAE
bordeaux.institutionArts et Métiers
hal.identifierhal-02187336
hal.version1
hal.origin.linkhttps://hal.archives-ouvertes.fr//hal-02187336v1
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