دورية أكاديمية
Inhibition of eIF5A hypusination reprogrammes metabolism and glucose handling in mouse kidney
| العنوان: | Inhibition of eIF5A hypusination reprogrammes metabolism and glucose handling in mouse kidney |
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| المؤلفون: | Cougnon, Marc, Carcy, Romain, Melis, Nicolas, Rubera, Isabelle, Duranton, Christophe, Dumas, Karine, Tanti, Jean‐françois, Pons, Catherine, Soubeiran, Nicolas, Shkreli, Marina, Hauet, Thierry, Pellerin, Luc, Giraud, Sébastien, Blondeau, Nicolas, Tauc, Michel, M., Pisani, Didier |
| المساهمون: | Laboratoire de PhysioMédecine Moléculaire (LP2M), Université Nice Sophia Antipolis (1965 - 2019) (UNS)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UniCA), Hôpital Pasteur Nice (CHU), National Cancer Institute Bethesda (NCI-NIH), National Institutes of Health Bethesda, MD, USA (NIH), Centre méditerranéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (1965 - 2019) (UNS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UniCA), Institut de Recherche sur le Cancer et le Vieillissement (IRCAN), Université Nice Sophia Antipolis (1965 - 2019) (UNS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UniCA), Ischémie Reperfusion en Transplantation d’Organes Mécanismes et Innovations Thérapeutiques U 1082 ( IRTOMIT Poitiers ), Université de Poitiers = University of Poitiers (UP)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de pharmacologie moléculaire et cellulaire (IPMC), ANR-19-CE18-0029,KIRI,Ciblage de l'agression ischémique, application à la transplantation d'organes(2019) |
| المصدر: | ISSN: 2041-4889 ; Cell Death and Disease ; https://hal.science/hal-03176556Test ; Cell Death and Disease, 2021, 12 (4), ⟨10.1038/s41419-021-03577-z⟩. |
| بيانات النشر: | HAL CCSD Nature Publishing Group |
| سنة النشر: | 2021 |
| المجموعة: | Université de Poitiers: Publications de nos chercheurs.ses (HAL) |
| مصطلحات موضوعية: | [SDV.BC]Life Sciences [q-bio]/Cellular Biology |
| الوصف: | International audience ; Inhibition of the eukaryotic initiation factor 5A activation by the spermidine analogue GC7 has been shown to protect proximal cells and whole kidneys against an acute episode of ischaemia. The highlighted mechanism involves a metabolic switch from oxidative phosphorylation toward glycolysis allowing cells to be transiently independent of oxygen supply. Here we show that GC7 decreases protein expression of the renal GLUT1 glucose transporter leading to a decrease in transcellular glucose flux. At the same time, GC7 modifies the native energy source of the proximal cells from glutamine toward glucose use. Thus, GC7 acutely and reversibly reprogrammes function and metabolism of kidney cells to make glucose its single substrate, and thus allowing cells to be oxygen independent through anaerobic glycolysis. The physiological consequences are an increase in the renal excretion of glucose and lactate reflecting a decrease in glucose reabsorption and an increased glycolysis. Such a reversible reprogramming of glucose handling and oxygen dependence of kidney cells by GC7 represents a pharmacological opportunity in ischaemic as well as hyperglycaemia-associated pathologies from renal origin. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| العلاقة: | info:eu-repo/semantics/altIdentifier/pmid/33731685; hal-03176556; https://hal.science/hal-03176556Test; https://hal.science/hal-03176556/documentTest; https://hal.science/hal-03176556/file/COUGNON%20et%20al%20rev%201.pdfTest; PUBMED: 33731685; PUBMEDCENTRAL: PMC7969969 |
| DOI: | 10.1038/s41419-021-03577-z |
| الإتاحة: | https://doi.org/10.1038/s41419-021-03577-zTest https://hal.science/hal-03176556Test https://hal.science/hal-03176556/documentTest https://hal.science/hal-03176556/file/COUGNON%20et%20al%20rev%201.pdfTest |
| حقوق: | info:eu-repo/semantics/OpenAccess |
| رقم الانضمام: | edsbas.52476094 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1038/s41419-021-03577-z |
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