Difference between revisions of "Sundaram 2023 Cell Metab"
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|journal=Cell Metab | |journal=Cell Metab | ||
|abstract=The peripheral nervous system harbors a remarkable potential to regenerate after acute nerve trauma. Full functional recovery, however, is rare and critically depends on peripheral nerve Schwann cells that orchestrate breakdown and resynthesis of myelin and, at the same time, support axonal regrowth. How Schwann cells meet the high metabolic demand required for nerve repair remains poorly understood. We here report that nerve injury induces adipocyte to glial signaling and identify the adipokine leptin as an upstream regulator of glial metabolic adaptation in regeneration. Signal integration by leptin receptors in Schwann cells ensures efficient peripheral nerve repair by adjusting injury-specific catabolic processes in regenerating nerves, including myelin autophagy and mitochondrial respiration. Our findings propose a model according to which acute nerve injury triggers a therapeutically targetable intercellular crosstalk that modulates glial metabolism to provide sufficient energy for successful nerve repair. | |abstract=The peripheral nervous system harbors a remarkable potential to regenerate after acute nerve trauma. Full functional recovery, however, is rare and critically depends on peripheral nerve Schwann cells that orchestrate breakdown and resynthesis of myelin and, at the same time, support axonal regrowth. How Schwann cells meet the high metabolic demand required for nerve repair remains poorly understood. We here report that nerve injury induces adipocyte to glial signaling and identify the adipokine leptin as an upstream regulator of glial metabolic adaptation in regeneration. Signal integration by leptin receptors in Schwann cells ensures efficient peripheral nerve repair by adjusting injury-specific catabolic processes in regenerating nerves, including myelin autophagy and mitochondrial respiration. Our findings propose a model according to which acute nerve injury triggers a therapeutically targetable intercellular crosstalk that modulates glial metabolism to provide sufficient energy for successful nerve repair. | ||
|keywords=Schwann cell, Adipocytes, Energy metabolism, Leptin, Leptin receptor, Metabolic adaptation, Mitochondrial respiration, Myelin autophagy, Myelinophagy, Nerve repair, Oxidative phosphorylation, Peripheral nerve injury, Regeneration, Remyelination | |||
|editor=[[Plangger M]] | |editor=[[Plangger M]] | ||
}} | }} | ||
Revision as of 16:24, 23 November 2023
| Sundaram VK, Schütza V, Schröter NH, Backhaus A, Bilsing A, Joneck L, Seelbach A, Mutschler C, Gomez-Sanchez JA, Schäffner E, Sánchez EE, Akkermann D, Paul C, Schwagarus N, Müller S, Odle A, Childs G, Ewers D, Kungl T, Sitte M, Salinas G, Sereda MW, Nave KA, Schwab MH, Ost M, Arthur-Farraj P, Stassart RM, Fledrich R (2023) Adipo-glial signaling mediates metabolic adaptation in peripheral nerve regeneration. https://doi.org/10.1016/j.cmet.2023.10.017 |
» Cell Metab [Epub ahead of print]. PMID: 37989315 Open Access
Sundaram VK, Schütza V, Schröter NH, Backhaus A, Bilsing A, Joneck L, Seelbach A, Mutschler C, Gomez-Sanchez JA, Schäffner E, Sánchez EE, Akkermann D, Paul C, Schwagarus N, Müller S, Odle A, Childs G, Ewers D, Kungl T, Sitte M, Salinas G, Sereda MW, Nave KA, Schwab MH, Ost M, Arthur-Farraj P, Stassart RM, Fledrich R (2023) Cell Metab
Abstract: The peripheral nervous system harbors a remarkable potential to regenerate after acute nerve trauma. Full functional recovery, however, is rare and critically depends on peripheral nerve Schwann cells that orchestrate breakdown and resynthesis of myelin and, at the same time, support axonal regrowth. How Schwann cells meet the high metabolic demand required for nerve repair remains poorly understood. We here report that nerve injury induces adipocyte to glial signaling and identify the adipokine leptin as an upstream regulator of glial metabolic adaptation in regeneration. Signal integration by leptin receptors in Schwann cells ensures efficient peripheral nerve repair by adjusting injury-specific catabolic processes in regenerating nerves, including myelin autophagy and mitochondrial respiration. Our findings propose a model according to which acute nerve injury triggers a therapeutically targetable intercellular crosstalk that modulates glial metabolism to provide sufficient energy for successful nerve repair. • Keywords: Schwann cell, Adipocytes, Energy metabolism, Leptin, Leptin receptor, Metabolic adaptation, Mitochondrial respiration, Myelin autophagy, Myelinophagy, Nerve repair, Oxidative phosphorylation, Peripheral nerve injury, Regeneration, Remyelination • Bioblast editor: Plangger M
Labels: MiParea: Respiration
HRR: Oxygraph-2k
2023-11
