Adipo-glial signaling mediates metabolic adaptation in peripheral nerve regeneration.

Autor:	Sundaram VK; Institute of Anatomy, Leipzig University, Leipzig, Germany; Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany., Schütza V; Institute of Anatomy, Leipzig University, Leipzig, Germany; Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany., Schröter NH; Institute of Anatomy, Leipzig University, Leipzig, Germany., Backhaus A; Institute of Anatomy, Leipzig University, Leipzig, Germany., Bilsing A; Institute of Anatomy, Leipzig University, Leipzig, Germany., Joneck L; Institute of Anatomy, Leipzig University, Leipzig, Germany., Seelbach A; Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany., Mutschler C; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK., Gomez-Sanchez JA; Instituto de Investigación Sanitaria y Biomédica de Alicante (ISABIAL), Alicante, Spain; Instituto de Neurociencias CSIC-UMH, San Juan de Alicante, Spain., Schäffner E; Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany., Sánchez EE; Institute of Anatomy, Leipzig University, Leipzig, Germany., Akkermann D; Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany., Paul C; Institute of Anatomy, Leipzig University, Leipzig, Germany., Schwagarus N; Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany., Müller S; Institute of Anatomy, Leipzig University, Leipzig, Germany., Odle A; Instituto de Neurociencias CSIC-UMH, San Juan de Alicante, Spain., Childs G; Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Markham, AR, USA., Ewers D; Max Planck Institute of Experimental Medicine, Göttingen, Germany; Klinik für Neurologie, Universitätsmedizin Göttingen (UMG), Göttingen, Germany., Kungl T; Institute of Anatomy, Leipzig University, Leipzig, Germany., Sitte M; NGS-Integrative Genomics Core Unit (NIG), Institute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany., Salinas G; NGS-Integrative Genomics Core Unit (NIG), Institute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany., Sereda MW; Max Planck Institute of Experimental Medicine, Göttingen, Germany; Klinik für Neurologie, Universitätsmedizin Göttingen (UMG), Göttingen, Germany., Nave KA; Max Planck Institute of Experimental Medicine, Göttingen, Germany., Schwab MH; Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany., Ost M; Institute of Anatomy, Leipzig University, Leipzig, Germany; Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany., Arthur-Farraj P; John Van Geest Centre for Brain Repair, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0PY, UK., Stassart RM; Paul Flechsig Institute of Neuropathology, University Clinic Leipzig, Leipzig, Germany. Electronic address: ruth.stassart@medizin.uni-leipzig.de., Fledrich R; Institute of Anatomy, Leipzig University, Leipzig, Germany. Electronic address: robert.fledrich@medizin.uni-leipzig.de.
Jazyk:	angličtina
Zdroj:	Cell metabolism [Cell Metab] 2023 Dec 05; Vol. 35 (12), pp. 2136-2152.e9. Date of Electronic Publication: 2023 Nov 20.
DOI:	10.1016/j.cmet.2023.10.017
Abstrakt:	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. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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