Coordinated Regulation of Myelination by Growth Factor and Amino-acid Signaling Pathways.
10.1007/s12264-022-00967-x
- Author:
Zhiwen YANG
1
;
Zongyan YU
2
;
Bo XIAO
3
Author Information
1. Shenzhen Key Laboratory of Gene Regulation and Systems Biology, Department of Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518000, China.
2. Shenzhen Key Laboratory of Gene Regulation and Systems Biology, Department of Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518000, China. 11849504@mail.sustech.edu.cn.
3. Shenzhen Key Laboratory of Gene Regulation and Systems Biology, Department of Biology, School of Life Sciences, Southern University of Science and Technology, Shenzhen, 518000, China. xiaob@sustech.edu.cn.
- Publication Type:Review
- Keywords:
GATOR2;
MIOS;
Oligodendrocyte;
RHEB;
Schwann cell;
lactate;
mTORC1;
mitochondria;
myelination
- MeSH:
Amino Acids;
Myelin Sheath/metabolism*;
Schwann Cells/metabolism*;
Oligodendroglia/metabolism*;
Signal Transduction;
Intercellular Signaling Peptides and Proteins/metabolism*
- From:
Neuroscience Bulletin
2023;39(3):453-465
- CountryChina
- Language:English
-
Abstract:
Myelin-forming oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS) are essential for structural and functional homeostasis of nervous tissue. Albeit with certain similarities, the regulation of CNS and PNS myelination is executed differently. Recent advances highlight the coordinated regulation of oligodendrocyte myelination by amino-acid sensing and growth factor signaling pathways. In this review, we discuss novel insights into the understanding of differential regulation of oligodendrocyte and Schwann cell biology in CNS and PNS myelination, with particular focus on the roles of growth factor-stimulated RHEB-mTORC1 and GATOR2-mediated amino-acid sensing/signaling pathways. We also discuss recent progress on the metabolic regulation of oligodendrocytes and Schwann cells and the impact of their dysfunction on neuronal function and disease.
