A molecular systems architecture of neuromuscular junction in amyotrophic lateral sclerosis

被引:0
|
作者
Ayyadurai, V. A. Shiva [1 ,2 ]
Deonikar, Prabhakar [1 ,2 ]
Kamm, Roger D. [3 ]
机构
[1] CytoSolve Inc, CytoSolve Res Div, Syst Biol Grp, Cambridge, MA 02138 USA
[2] Int Ctr Integrat Syst, Open Sci Inst, Cambridge, MA 02138 USA
[3] MIT, Dept Biol Engn & Mech Engn, Cambridge, MA USA
关键词
POTENTIAL THERAPEUTIC TARGET; SKELETAL-MUSCLE ATROPHY; MOUSE MODEL; SPINAL-CORD; ER STRESS; ALS; RECEPTOR; C9ORF72; ACTIVATION; COMPLEX;
D O I
10.1038/s41540-025-00501-5
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
A molecular systems architecture is presented for the neuromuscular junction (NMJ) in order to provide a framework for organizing complexity of biomolecular interactions in amyotrophic lateral sclerosis (ALS) using a systematic literature review process. ALS is a fatal motor neuron disease characterized by progressive degeneration of the upper and lower motor neurons that supply voluntary muscles. The neuromuscular junction contains cells such as upper and lower motor neurons, skeletal muscle cells, astrocytes, microglia, Schwann cells, and endothelial cells, which are implicated in pathogenesis of ALS. This molecular systems architecture provides a multi-layered understanding of the intra- and inter-cellular interactions in the ALS neuromuscular junction microenvironment, and may be utilized for target identification, discovery of single and combination therapeutics, and clinical strategies to treat ALS.
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页数:20
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