Abstract：Autophagy is an important process which is widespread in eukaryotic cells, and it is closely associated with cell growth and development as well as a series of diseases. Autophagy lets the autophagosomes devour and degrade the damaged organelles and abnormal proteins, and then the released small molecules which are useful substances for the cells are employed for secondary use so as to maintain intracellular homeostasis. Not only is autophagy a protective mechanism, it is also considered to be a mechanism of death associated with programmed cell death. Autophagy due to the features of "double-edged sword", plays an important role in the nervous system damage and neurodegenerative diseases (such as Alzheimer's disease, Parkinson's disease and Huntington's disease). It is of great value to intensively study the regulating mechanism of autophagy for preventing and treating neurodegenerative diseases.
杨越, 龙鼎新. 自噬与神经系统退行性疾病的研究进展[J]. 实用预防医学, 2018, 25(5): 638-641.
YANG Yue, LONG Ding-xin. Research progress on autophagy and nervous system degenerative diseases. , 2018, 25(5): 638-641.
[1] Kochergin IA, Zakharova MN. The role of autophagy in neurodegenerative diseases [J]. Neurochem J, 2016, 10(1):7-18. [2] Mizushima N, Levine B, Cuervo AM, et al. Autophagy fights disease through cellular self-digestion [J]. Nature, 2008, 451(7182):1069-1075. [3] Bernard A, Jin M, Xu Z, et al. A large-scale analysis of autophagy-related gene expression identifies new regulators of autophagy [J]. Autophagy, 2015, 11(11):2114-2122. [4] Randhawa R, Sehgal M, Singh TR, et al. Unc-51 like kinase 1 (ULK1) in silico analysis for biomarker identification:a vital component of autophagy [J]. Gene, 2015, 562(1):40-49. [5] Yang Z, Klionsky DJ. Eaten alive:a history of macroautophagy[J]. Nat Cell Biol, 2010,12(9):814-822. [6] Rahman MA, Rhim H. Therapeutic implication of autophagy in neurodegenerative diseases[J]. BMB Rep, 2017. [7] Scala CD, Chahinian H, Yahi N, et al. Interaction of Alzheimer’s β-amyloid peptides with cholesterol: mechanistic insights into amyloid poreformation[J]. Biochemistry, 2014, 53(28):4489-4502. [8] Nixon RA, Yang DS. Autophagy failure in Alzheimer's disease-locating the primary defect[J]. Neurobiol Dis, 2011, 43(43):38-45. [9] Salminen A, Kai K, Haapasalo A, et al. Emerging role of p62/sequestosome-1 in the pathogenesis of Alzheimer's disease [J]. Prog Neurobiol, 2012, 96(1):87-95. [10] Tanji K, Miki Y, Ozaki T, et al. Phosphorylation of serine 349 of p62 in Alzheimer’s disease brain [J]. Acta Neuropathol Commun, 2014, 2(1):50. [11] Cuyvers E, van der Zee J, Bettens K, et al. Genetic variability in SQSTM1 and risk of early-onset Alzheimer dementia :a European early-onset dementia consortium study[J]. Neurobiol Aging, 2015, 36(5):e15-e22. [12] Kasturi R, Oishee C, Debashis M. Interaction of Grb2 SH3 domain with UVRAG in an Alzheimer's disease-like scenario [J]. Biochem Cell Biol, 2014, 92(3):219-225. [13] Lucin KM, O’brien CE, Bieri G, et al. Microglial beclin 1 regulates retromer trafficking and phagocytosis and is impaired in Alzheimer’s disease [J]. Neuron, 2013, 79(5):873-886. [14] Saha S, Ash PEA, Gowda V, et al. Mutations in LRRK2 potentiate age-related impairment of autophagic flux [J]. Mol Neurodegener, 2015, 10(1):26. [15] Meka DP, Mullerrischart AK, Nidadavolu P, et al. Parkin cooperates with GDNF/RET signaling to prevent dopaminergic neuron degeneration [J]. J Clin Invest, 2015, 125(5):1873-1885. [16] Nascimentoferreira I, Santosferreira T, Sousaferreira L, et al. Overexpression of the autophagic beclin-1 protein clears mutant ataxin-3 and alleviates Machado–Joseph disease [J]. Brain, 2011, 134(5):1400-1415. [17] Menzies FM, Fleming A, Caricasole A, et al. Autophagy and neurodegeneration: pathogenic mechanisms and therapeutic opportunities [J]. Neuron, 2017, 93(5):1015-1034. [18] Jiang W, Wwi W, Gaertig MA, et al. Therapeutic effect of berberine on Huntington's disease transgenic mouse model [J]. PLoS One, 2015, 10(7):e0134142. [19] Mealer RG, Murray AJ, Shahani N, et al. Rhes, a striatal-selective protein implicated in Huntington disease, binds beclin-1 and activates autophagy [J]. J Biol Chem, 2014, 289(6):3547-3554. [20] Jin HS, Shim JH, Kim KH, et al. Neuronal autophagy and neurodegenerative diseases [J]. Exp Mol Med, 2011, 44(2):89. [21] 贺丽. 自噬在TOCP诱发成年母鸡迟发性神经毒性中的作用探讨 [D]. 衡阳:南华大学, 2013. [22] Long DX, Hu D, Wang P, et al. Induction of autophagy in human neuroblastoma SH-SY5Y cells by tri-ortho-cresyl phosphate [J]. Mol Cell Biochem, 2014, 396(1):33-40. [23] Song F, Han X, Zeng T, et al. Changes in beclin-1 and micro-calpain expression in tri-ortho-cresyl phosphate-induced delayed neuropathy [J]. Toxicol Lett, 2012, 210(3):276-284. [24] Xie Y, Zhou B, Lin MY, et al. Progressive endolysosomal deficits impair autophagic clearance beginning at early asymptomatic stages in fALS mice[J]. Autophagy,2015, 11(10):1934-1936. [25] Kuzma-Kozakiewicz M, Chudy A, Kazmierczak B, et al. Dynactin deficiency in the CNS of humans with sporadic ALS and mice with genetically determined motor neuron degeneration [J]. Neurochem Res, 2013, 38(12):2463-2473. [26] Khaminets A, Behl C, Dikic I. Ubiquitin-dependent and independent signals in selective autophagy [J]. Trends Cell Biol, 2016, 26(1):6-16. [27] Shen WC, Li HY, Chen GC, et al. Mutations in the ubiquitin-binding domain of OPTN/optineurin interfere with autophagy-mediated degradation of misfolded proteins by a dominant-negative mechanism[J]. Autophagy, 2015, 11(4):685-700. [28] Durcan TM, Kontogiannea M, Bedard N, et al. Ataxin-3 deubiquitination is coupled to parkin ubiquitination via E2 ubiquitin-conjugating enzyme [J]. J Biol Chem, 2012, 287(1):531-541.
2018, Vol. 25 
