德国莱比锡大学Robert Fledrich和德国莱比锡大学诊所Ruth M. Stassart共同合作，最近取得重要工作进展。他们研究发现，脂肪-胶质细胞信号介导周围神经再生过程中的代谢适应。相关研究成果2023年11月20日在线发表于《细胞—代谢》杂志上。

据介绍，急性神经损伤后，外周神经系统具有显著的再生潜力。然而，完全功能恢复是罕见的，关键取决于外周神经施旺细胞，这些细胞协调髓鞘的分解和再合成，同时支持轴突再生。施旺细胞如何满足神经修复所需的高代谢需求仍知之甚少。

研究人员报道了神经损伤诱导脂肪细胞到神经胶质的信号传导，并确定脂肪因子瘦素是再生中神经胶质代谢适应的上游调节因子。施旺细胞中瘦素受体的信号整合通过调节再生神经中损伤特异性分解代谢过程，包括髓鞘自噬和线粒体呼吸，确保有效的外周神经修复。

总之，这一研究结果提出了一个模型，根据该模型，急性神经损伤可触发治疗靶向的细胞间相互作用，调节神经胶质代谢，为成功的神经修复提供足够的能量。

附：英文原文

Title: Adipo-glial signaling mediates metabolic adaptation in peripheral nerve regeneration

Author: Venkat Krishnan Sundaram, Vlad Schütza, Nele H. Schrter, Aline Backhaus, Annika Bilsing, Lisa Joneck, Anna Seelbach, Clara Mutschler, Jose A. Gomez-Sanchez, Erik Schffner, Eva Ernst Sánchez, Dagmar Akkermann, Christina Paul, Nancy Schwagarus, Silvana Müller, Angela Odle, Gwen Childs, David Ewers, Theresa Kungl, Maren Sitte, Gabriela Salinas, Michael W. Sereda, Klaus-Armin Nave, Markus H. Schwab, Mario Ost, Peter Arthur-Farraj, Ruth M. Stassart, Robert Fledrich

Issue&Volume: 2023-11-20

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.

DOI: 10.1016/j.cmet.2023.10.017

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00386-8