Xie Yinyin, Sun Wenlin, Han Aoya, Zhou Xinru, Zhang Shijie, Shen Changchang, Xie Yi, Wang Cui, Xie Nanchang
Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Department of Clinical Laboratory, The First Affiliated Hospital of Zhengzhou University, Key Clinical Laboratory of Henan Province, Zhengzhou, China.
Front Mol Neurosci. 2025 Jan 14;17:1527013. doi: 10.3389/fnmol.2024.1527013. eCollection 2024.
Mitochondria and lysosomes are critical for neuronal homeostasis, as highlighted by their dysfunction in various neurological diseases. Recent studies have identified dynamic membrane contact sites between mitochondria and lysosomes, independent of mitophagy and the lysosomal degradation of mitochondrial-derived vesicles (MDVs), allowing bidirectional crosstalk between these cell compartments, the dynamic regulation of organelle networks, and substance exchanges. Emerging evidence suggests that abnormalities in mitochondria-lysosome contact sites (MLCSs) contribute to neurological diseases, including Parkinson's disease, Charcot-Marie-Tooth (CMT) disease, lysosomal storage diseases, and epilepsy. This article reviews recent research advances regarding the tethering processes, regulation, and function of MLCSs and their role in neurological diseases.
线粒体和溶酶体对神经元内环境稳定至关重要，各种神经疾病中它们的功能障碍就突出了这一点。最近的研究发现了线粒体和溶酶体之间动态的膜接触位点，这些位点独立于线粒体自噬和线粒体衍生囊泡（MDV）的溶酶体降解，使得这些细胞区室之间能够进行双向串扰、细胞器网络的动态调节以及物质交换。新出现的证据表明，线粒体-溶酶体接触位点（MLCS）异常会导致神经疾病，包括帕金森病、夏科-马里-图斯（CMT）病、溶酶体贮积病和癫痫。本文综述了关于MLCS的连接过程、调节、功能及其在神经疾病中的作用的最新研究进展。
