Research progress in the autophagy related mechanisms in traumatic brain injury

doi:10.3969/j.issn.1006-7795.2016.06.015

Abstract

Abstract: Traumatic brain injury (TBI) is one of the most important causes of disability of the young people and adults around the world, which caused high mortality and the survivors often accompanied sequelae of physical disability, mental disability and so on. TBI brings a heavy burden to the society development. Autophagy is a hot research field in recent years. Although the study on the mechanism of autophagy changes in the secondary damage induced by TBI has been gradually increasing in recent years, there are still many mechanisms of autophagy to be elucidated. The main aim of this review is to elaborate on the changes of autophagy related mechanism after TBI.

Key words: traumatic brain injury, autophagy, autophagy related mechanisms

CLC Number:

R651.1

Liu Yuan, Wang Rong. Research progress in the autophagy related mechanisms in traumatic brain injury[J]. Journal of Capital Medical University, 2016, 37(6): 794-798.

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URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2016.06.015

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2016/V37/I6/794

References

[1] Gyoneva S, Ransohoff R M. Inflammatory reaction after traumatic brain injury: therapeutic potential of targeting cell-cell communication by chemokines[J]. Trends Pharmacol Sci, 2015, 36(7): 471-480.
[2] Ansari M A, Roberts K N, Scheff S W. Oxidative stress and modification of synaptic proteins in hippocampus after traumatic brain injury[J]. Free Radical Biol Med, 2008, 45(4): 443-452.
[3] Shin S S, Dixon C E. Alterations in cholinergic pathways and therapeutic strategies targeting cholinergic system after traumatic brain injury[J]. J Neurotrauma, 2015, 32(19): 1429-1440.
[4] Kilbaugh T J, Karlsson M, Duhaime A C, et al. Mitochondrial response in a toddler-aged swine model following diffuse non-impact traumatic brain injury[J]. Mitochondrion, 2016, 26: 19-25.
[5] Yao J, Zheng K, Zhang X. Rosiglitazone exerts neuroprotective effects via the suppression of neuronal autophagy and apoptosis in the cortex following traumatic brain injury[J]. Mol Med Rep, 2015, 12(5): 6591-6597.
[6] Chien M Y, Chuang C H, Chern C M, et al. Salvianolic acid A alleviates ischemic brain injury through the inhibition of inflammation and apoptosis and the promotion of neurogenesis in mice[J]. Free Rad Biol Med, 2016, 99: 508-519.
[7] Diskin T, Tal-Or P, Erlich S, et al. Closed head injury induces upregulation of Beclin 1 at the cortical site of injury[J]. J Neurotraum, 2005, 22(7): 750-762.
[8] Park Y, Liu C, Luo T, et al. Chaperone-mediated autophagy after traumatic brain injury[J]. J Neurotraum, 2015, 32(19): 1449-1457.
[9] Cordaro M, Impellizzeri D, Paterniti I, et al. Neuroprotective effects of Co-ultraPEALut on secondary inflammatory process and autophagy involved in traumatic brain injury[J]. J Neurotraum, 2016, 33(1): 132-146.
[10] Zhang L, Ding K, Wang H, et al. Traumatic brain injury-induced neuronal apoptosis is reduced through modulation of PI3K and autophagy pathways in mouse by FTY720[J]. Cell Molecular Neurobiol, 2016, 36(1): 131-142.
[11] Rubinsztein D C, DiFiglia M, Heintz N, et al. Autophagy and its possible roles in nervous system diseases, damage and repair[J]. Autophagy, 2005, 1(1): 11-22.
[12] Liu C L, Chen S, Dietrich D, et al. Changes in autophagy after traumatic brain injury[J]. J Cereb Blood Flow Metabol, 2008, 28(4): 674-683.
[13] Sakai K, Fukuda T, Iwadate K. Immunohistochemical analysis of the ubiquitin proteasome system and autophagy lysosome system induced after traumatic intracranial injury: association with time between the injury and death[J]. The Am J Forensic Med Pathol, 2014, 35(1): 38-44.
[14] Luo C L, Li B X, Li Q Q, et al. Autophagy is involved in traumatic brain injury-induced cell death and contributes to functional outcome deficits in mice[J]. Neuroscience, 2011, 184: 54-63.
[15] Viscomi M T, D'Amelio M, Cavallucci V, et al. Stimulation of autophagy by rapamycin protects neurons from remote degeneration after acute focal brain damage[J]. Autophagy, 2012, 8(2): 222-235.
[16] Klionsky D J, Abdalla F C, Abeliovich H, et al. Guidelines for the use and interpretation of assays for monitoring autophagy[J]. Autophagy, 2012, 8(4): 445-544.
[17] Sarkar C, Zhao Z, Aungst S, et al. Impaired autophagy flux is associated with neuronal cell death after traumatic brain injury[J]. Autophagy, 2014, 10(12): 2208-2222.
[18] Morrison Ⅲ B, Elkin B S, Dollé J P, et al. In vitro models of traumatic brain injury[J]. Ann Rev Biomed Engineering, 2011, 13: 91-126.
[19] Bejarano E, Yuste A, Patel B, et al. Connexins modulate autophagosome biogenesis[J]. Nat Cell Biol, 2014, 16(5): 401.
[20] Sun L Q, Gao J L, Cui C M, et al. Astrocytic p-connexin 43 regulates neuronal autophagy in the hippocampus following traumatic brain injury in rats[J]. Mol Med Rep, 2014, 9(1): 77-82.
[21] Bigford G E, Alonso O F, Dietrich W D, et al. A novel protein complex in membrane rafts linking the NR2B glutamate receptor and autophagy is disrupted following traumatic brain injury[J]. J Neurotraum, 2009, 26(5): 703-720.
[22] Lin C J, Chen T H, Yang L Y, et al. Resveratrol protects astrocytes against traumatic brain injury through inhibiting apoptotic and autophagic cell death[J]. Cell Death Dis, 2014, 5(3): e1147.
[23] Yamashima T, Oikawa S. The role of lysosomal rupture in neuronal death[J]. Prog Neurobiol, 2009, 89(4): 343-358.
[24] Bové J, Martínez-Vicente M, Dehay B, et al. BAX channel activity mediates lysosomal disruption linked to Parkinson disease[J]. Autophagy, 2014, 10(5): 889-900.
[25] Sabirzhanov B, Zhao Z, Stoica B A, et al. Downregulation of miR-23a and miR-27a following experimental traumatic brain injury induces neuronal cell death through activation of proapoptotic Bcl-2 proteins[J]. J Neurosci, 2014, 34(30): 10055-10071.
[26] Filomeni G, De Zio D, Cecconi F. Oxidative stress and autophagy: the clash between damage and metabolic needs[J]. Cell Death Differ, 2015, 22(3): 377-388.
[27] Lipinski M M, Zheng B, Lu T, et al. Genome-wide analysis reveals mechanisms modulating autophagy in normal brain aging and in Alzheimer's disease[J]. Natl Acad Sci USA, 2010, 107(32): 14164-14169.
[28] Zmijewski J W, Banerjee S, Bae H, et al. Exposure to hydrogen peroxide induces oxidation and activation of AMP-activated protein kinase[J]. J Biol Chem, 2010, 285(43): 33154-33164.
[29] Sarkar S, Korolchuk V I, Renna M, et al. Complex inhibitory effects of nitric oxide on autophagy[J]. Mol Cell, 2011, 43(1): 19-32.
[30] You Z, Savitz S I, Yang J, et al. Necrostatin-1 reduces histopathology and improves functional outcome after controlled cortical impact in mice[J]. J Cerebr Blood F Met, 2008, 28(9): 1564-1573.
[31] Erlich S, Alexandrovich A, Shohami E, et al. Rapamycin is a neuroprotective treatment for traumatic brain injury[J]. Neurobiol Dis, 2007, 26(1): 86-93.
[32] Puyal J, Vaslin A, Mottier V, et al. Postischemic treatment of neonatal cerebral ischemia should target autophagy[J]. Ann Neurol, 2009, 66(3): 378-389.
[33] 肖遥,徐善才,史怀璋. 自噬在蛛网膜下腔出血后早期脑损伤中作用的研究进展[J]. 中国脑血管病杂志,2013,10(10):553-556.
[34] 胡瑞, 张晓云,晏雪,等. 脑出血后炎性反应机制的研究进展[J]. 中国脑血管病杂志,2015,12(7):370-374.