Citation

Liu FS, Jiang C, Li Z, Wang XB, Li J, Wang B, Lv GH, Liu FB. Neurochem. Res. 2022; ePub(ePub): ePub.

Copyright

(Copyright © 2022, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s11064-022-03768-w

PMID

36315370

Abstract

Spinal cord injury (SCI), resulting in damage of the normal structure and function of the spinal cord, would do great harm to patients, physically and psychologically. The mechanism of SCI is very complex. At present, lots of studies have reported that autophagy was involved in the secondary injury process of SCI, and several researchers also found that calcium ions (Ca(2+)) played an important role in SCI by regulating necrosis, autophagy, or apoptosis. However, to our best of knowledge, no studies have linked the spinal cord mechanical injury, intracellular Ca(2+), and autophagy in series. In this study, we have established an in vitro model of SCI using neural cells from fetal rats to explore the relationship among them, and found that mechanical injury could promote the intracellular Ca(2+) concentration, and the increased Ca(2+) level activated autophagy through the CaMKKβ/AMPK/mTOR pathway. Additionally, we found that apoptosis was also involved in this pathway. Thus, our study provides new insights into the specific mechanisms of SCI and may open up new avenues for the treatment of SCI.

Language: en

Keywords

apoptosis; autophagy; calcium ions; calmodulin-dependent protein kinase kinaseβ; mechanical injury; spinal cord injury