Autophagy in neural stem cells and glia for brain health and diseases.
Autophagy in neural stem cells and glia for brain health and diseases.
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DOI：
10.4103/1673-5374.382227
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发表时间：
2024-04
影响因子：
6.1
通讯作者：
Wang C
中科院分区：
文献类型：
--
作者：
Nagayach A;Wang C
自噬是一个多方面的细胞过程，它不仅维持大脑的稳态和适应性反应，而且还动态地参与神经细胞生成，成熟和存活的调节。自噬为神经干细胞的发育提供了能量利用和微环境。自噬在细胞分化过程中仲裁结构和功能重塑。自噬在维持神经干细胞的干性和稳态方面也起着不可或缺的作用，在基本的脑生理过程中，也在疾病的煽动和进展中起着不可或缺的作用。直到最近，研究才开始阐明大脑中胶质细胞（小胶质细胞，星形胶质细胞和少突胶质细胞）的自噬调节。尽管神经胶质细胞对神经发育、突触功能、脑代谢、细胞碎片清除和受损或损伤组织的恢复的各个方面的影响是毋庸置疑的，但其获得的关注相对较少。因此，本文综述了自噬在神经干细胞和神经胶质细胞调节中的作用，以及自噬在正常脑功能、神经发育障碍和神经退行性疾病中的作用。这篇综述将为研究脑疾病的病理机制和开发脑疾病的治疗方法提供一个具体的战略方法。
Autophagy is a multifaceted cellular process that not only maintains the homeostatic and adaptive responses of the brain but is also dynamically involved in the regulation of neural cell generation, maturation, and survival. Autophagy facilities the utilization of energy and the microenvironment for developing neural stem cells. Autophagy arbitrates structural and functional remodeling during the cell differentiation process. Autophagy also plays an indispensable role in the maintenance of stemness and homeostasis in neural stem cells during essential brain physiology and also in the instigation and progression of diseases. Only recently, studies have begun to shed light on autophagy regulation in glia (microglia, astrocyte, and oligodendrocyte) in the brain. Glial cells have attained relatively less consideration despite their unquestioned influence on various aspects of neural development, synaptic function, brain metabolism, cellular debris clearing, and restoration of damaged or injured tissues. Thus, this review composes pertinent information regarding the involvement of autophagy in neural stem cells and glial regulation and the role of this connexion in normal brain functions, neurodevelopmental disorders, and neurodegenerative diseases. This review will provide insight into establishing a concrete strategic approach for investigating pathological mechanisms and developing therapies for brain diseases.
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影响因子：
5.9
作者：
Chandrasekaran A;Dittlau KS;Corsi GI;Haukedal H;Doncheva NT;Ramakrishna S;Ambardar S;Salcedo C;Schmidt SI;Zhang Y;Cirera S;Pihl M;Schmid B;Nielsen TT;Nielsen JE;Kolko M;Kobolák J;Dinnyés A;Hyttel P;Palakodeti D;Gorodkin J;Muddashetty RS;Meyer M;Aldana BI;Freude KK
通讯作者：
Freude KK
AMP激活的蛋白激酶对ULK1（HATG1）的磷酸化将能量传感连接到线粒体。
DOI：
10.1126/science.1196371
发表时间：
2011-01-28
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Egan DF;Shackelford DB;Mihaylova MM;Gelino S;Kohnz RA;Mair W;Vasquez DS;Joshi A;Gwinn DM;Taylor R;Asara JM;Fitzpatrick J;Dillin A;Viollet B;Kundu M;Hansen M;Shaw RJ
通讯作者：
Shaw RJ
影响因子：
16.6
作者：
Choi, Insup;Zhang, Yuanxi;Yue, Zhenyu
通讯作者：
Yue, Zhenyu
影响因子：
13.3
作者：
Cho, Mi-Hyang;Cho, Kwangmin;Yoon, Seung-Yong
通讯作者：
Yoon, Seung-Yong
影响因子：
4.3
作者：
Rodriguez-Bodero, Ane;Encinas-Perez, Juan Manuel
通讯作者：
Encinas-Perez, Juan Manuel