Ca2+ Regulates Autophagy Through CaMKKβ/AMPK/mTOR Signaling Pathway in Mechanical Spinal cord Injury: An in vitro Study

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,Chang Jiang,Zheng Li,Xiaobin Wang,Jing Li,Bing Wang,Guohua Lv,Fu-Bing Liu
出处
期刊:Neurochemical Research [Springer Science+Business Media]
卷期号:48 (2): 447-457 被引量:6
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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