自噬
脊髓损伤
安普克
PI3K/AKT/mTOR通路
细胞生物学
细胞凋亡
细胞内
神经保护
脊髓
神经科学
信号转导
化学
生物
医学
磷酸化
蛋白激酶A
生物化学
作者
Fusheng Liu,Jiang Chang,Zheng Li,Xiaobin Wang,Jing Li,Bing Wang,Guohua Lv,Fu-Bing Liu
标识
DOI:10.1007/s11064-022-03768-w
摘要
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 (Ca2+) 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 Ca2+, 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 Ca2+ concentration, and the increased Ca2+ 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.
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