中枢髓鞘是由少突胶质细胞突起包绕轴突形成的螺旋样多层生物膜结构，是维持神经正常生理活动的基础。脂质是髓鞘的主要成分，但是目前尚不清楚髓鞘特征性脂质代谢在髓鞘形成中的作用。我们的前期研究显示：脂酰辅酶A硫酯酶7（Acot7）在少突胶质细胞中特异性表达；在小鼠白质发育成熟阶段和脱髓鞘后再髓鞘化过程中，Acot7的表达量显著升高；Acot7对体外原代培养的少突胶质前体细胞分化成熟，具有促进作用；在少突胶质细胞中条件性敲除Acot7，会显著抑制小鼠中枢髓鞘生成。这些研究结果强烈提示Acot7在髓鞘形成中具有重要作用。本项目拟在前期实验基础上，深入、系统地分析Acot7在中枢髓鞘发育和再生过程中的作用，并阐明其发挥作用的机制。这项研究不仅有可能揭示Acot7的新功能，而且有助于深入认识髓鞘形成的调控机制，并可能为脱髓鞘相关疾病的治疗研究提供新思路。

Myelin, formed by the wrapping of axons with the processes of oligodendrocytes, is vital for maintaining normal physiological function in the central nerve system. Lipid is the main component of myelin, but the role of synthesis and metabolism of myelin lipid in myelination is not fully understood yet. In the preliminary study. we found that Acyl-CoA thioesterase 7 (ACOT7), a major isoform of the ACOT family, was highly expressed in the oligodendrocytes in vitro and in vivo. The expression of Acot7 was significantly increased during the development of mouse white matter and as the remyelination occurred after demyelination. Acot7 was found to promote the differentiation and maturation of primary cultured oligodendrocyte precursor cells. Importantly, after conditional knockout of Acot7 in oligodendrocytes, the myelin generation during development was greatly inhibited. Our preliminary data strongly indicate that Acot7 play a crucial role in myelination. In this proposal, we aim to further analyze the role and the underlying mechanism of Acot7 in myelination. The goal of this research is to establish the role of Acot7 in the regulation of myelination and to open up new possibilities to achieve successful therapeutic explorations for demyelinating diseases.