Syntaphilin mediates axonal growth and synaptic changes through regulation of mitochondrial transport: a potential pharmacological target for neurodegenerative diseases
Syntaphilin mediates axonal growth and synaptic changes through regulation of mitochondrial transport: a potential pharmacological target for neurodegenerative diseases
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DOI：
10.1080/1061186x.2023.2230522
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发表时间：
2023-06
影响因子：
4.5
通讯作者：
Qing-Yun Wu;Hui-Lin Liu;Hai-yan Wang;Kaiyuan Hu;Ping Liao;Sen Li;Z. Long;Xiu-Min Lu;
中科院分区：
文献类型：
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作者：
Qing-Yun Wu;Hui-Lin Liu;Hai-yan Wang;Kaiyuan Hu;Ping Liao;Sen Li;Z. Long;Xiu-Min Lu;
摘要线粒体是维持神经元生长和突触功能的重要能量来源。神经元具有独特的形态特征，这使得适当地调节线粒体运输对于满足其能量需求至关重要。突触素(SNPH)能够特异性地靶向轴突线粒体的外膜，将它们固定在微管上，从而阻止它们的运输。SNPH还与其他线粒体蛋白相互作用，调节线粒体的运输。SNPH介导的线粒体转运和锚定的调节对于神经元发育过程中的轴突生长、神经元突触活动过程中的ATP水平的维持以及损伤后成熟神经元的再生都是不可或缺的。精确阻断SNPH可能是治疗神经退行性疾病和相关精神障碍的有效策略。
Abstract Mitochondria are a crucial energy source for maintaining neuronal growth and synaptic function. Neurons possess unique morphological characteristics, which make the proper regulation of mitochondrial transport essential for meeting their energy demands. Syntaphilin (SNPH) is capable of specifically targeting the outer membrane of axonal mitochondria, anchoring them to microtubules, and thereby preventing their transport. SNPH also interacts with other mitochondrial proteins to regulate mitochondrial transport. The regulation of mitochondrial transport and anchoring mediated by SNPH is indispensable for axonal growth during neuronal development, maintenance of ATP levels during neuronal synaptic activity, and regeneration of mature neurons following damage. Precise blocking of SNPH may be an effective therapeutic strategy for neurodegenerative diseases and related mental disorders.