德國萊比錫大學(xué)Robert Fledrich和德國萊比錫大學(xué)診所Ruth M. Stassart共同合作，最近取得重要工作進(jìn)展。他們研究發(fā)現(xiàn)，脂肪-膠質(zhì)細(xì)胞信號介導(dǎo)周圍神經(jīng)再生過程中的代謝適應(yīng)。相關(guān)研究成果2023年11月20日在線發(fā)表于《細(xì)胞—代謝》雜志上。
據(jù)介紹，急性神經(jīng)損傷后，外周神經(jīng)系統(tǒng)具有顯著的再生潛力。然而，完全功能恢復(fù)是罕見的，關(guān)鍵取決于外周神經(jīng)施旺細(xì)胞，這些細(xì)胞協(xié)調(diào)髓鞘的分解和再合成，同時支持軸突再生。施旺細(xì)胞如何滿足神經(jīng)修復(fù)所需的高代謝需求仍知之甚少。
研究人員報道了神經(jīng)損傷誘導(dǎo)脂肪細(xì)胞到神經(jīng)膠質(zhì)的信號傳導(dǎo)，并確定脂肪因子瘦素是再生中神經(jīng)膠質(zhì)代謝適應(yīng)的上游調(diào)節(jié)因子。施旺細(xì)胞中瘦素受體的信號整合通過調(diào)節(jié)再生神經(jīng)中損傷特異性分解代謝過程，包括髓鞘自噬和線粒體呼吸，確保有效的外周神經(jīng)修復(fù)。
總之，這一研究結(jié)果提出了一個模型，根據(jù)該模型，急性神經(jīng)損傷可觸發(fā)治療靶向的細(xì)胞間相互作用，調(diào)節(jié)神經(jīng)膠質(zhì)代謝，為成功的神經(jīng)修復(fù)提供足夠的能量。
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.
來源：科學(xué)網(wǎng)
原標(biāo)題：脂肪-膠質(zhì)細(xì)胞信號介導(dǎo)周圍神經(jīng)再生過程中的代謝適應(yīng)
作者：小柯
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