自噬与阿尔茨海默病相关性研究
Research Progress of the Role of Autophagy in Alzheimer’s Disease
DOI: 10.12677/ACM.2017.75049, PDF,   
作者: 毕薪燃, 李 舒：青岛大学附属医院神经内科，山东 青岛
关键词: 自噬；阿尔茨海默氏病；Autophagy； Alzheimer’s Disease
摘要: 自噬为真核细胞独有的代谢过程，基础自噬通过清除衰老的细胞器和异常堆积的蛋白，保证其正常的细胞功能。然而失调的自噬或者过多的自噬都会导致细胞死亡。在AD患者或转基因AD鼠的神经细胞中存在大量的自噬囊泡，表明自噬可能参与了阿尔茨海默病的发生、发展。因此，明确自噬在AD 发病不同阶段的确切作用可能有助于发现更为有效的治疗靶点。
Abstract: Autophagy is a unique metabolic process for eukaryotic cells, and basal autophagy protects its normal cellular function by removing damaged organelles and abnormally aggregated proteins. However, abnormal autophagy or excessive autophagy can lead to cell death. There are a large number of autophagic vesicles in the nerve cells of Alzheimer’s patients or transgenic mice, sug-gesting that autophagy may be involved in the development and progression of Alzheimer’s disease. Thus, the exact role of autophagy at different stages of AD pathogenesis may help to find more effective therapeutic targets.
文章引用：毕薪燃, 李舒. 自噬与阿尔茨海默病相关性研究[J]. 临床医学进展, 2017, 7(5): 295-298. https://doi.org/10.12677/ACM.2017.75049

参考文献

[1] Bartel, D.P. (2004) MicroRNAs: Genomics, Biogenesis, Mechanism, and Function. Cell, 116, 281-297.
[2] Di Leva, G. and Croce, C.M. (2010) Roles of Small RNAs in Tumor Formation. Trends in Molecular Medicine, 16, 257-267.
[3] Calin, G.A., Dumitru, C.D., Shimizu, M., Bichi, R., Zupo, S., Noch, E., Aldler, H., Rattan, S., Keating, M., Rai, K., Rassenti, L., Kipps, T., Negrini, M., Bullrich, F. and Croce, C.M. (2002) Nonlinear Partial Differential Equations and Applications: Frequent Deletions and Down-Regulation of Micro-RNA Genes miR15 and miR16 at 13q14 in Chronic Lymphocytic Leukemia. Proceedings of the National Academy of Sciences of the USA, 99, 15524-15529.
[4] Cimmino, A., Calin, G.A., Fabbri, M., Iorio, M.V., Ferracin, M., Shimizu, M., Wojcik, S.E., Aqeilan, R.I., Zupo, S., Dono, M., Rassenti, L., Alder, H., Volinia, S., Liu, C.-G., Kipps, T.J., Negrini, M. and Croce, C.M. (2005) miR-15 and miR-16 Induce Apoptosis by Targeting BCL2. Proceedings of the National Academy of Sciences of the USA, 102, 13944-13949.
[5] Martens-Uzunova, E.S., Jalava, S.E., Dits, N.F., van Leenders, G.J., Møller, S., Trapman, J., Bangma, C.H., Litman, T., Visakorpi, T. and Jenster, G. (2012) Diagnostic and Prognostic Signatures from the Small Non-Coding RNA Tran-scriptome in Prostate Cancer. Oncogene, 31, 978-991.
[6] Farazi, T.A., Horlings, H.M., Ten Hoeve, J.J., Mihailovic, A., Halfwerk, H., Morozov, P., Brown, M., Hafner, M., Reyal, F., van Kouwenhove, M., Kreike, B., Sie, D., Hovestadt, V., Wessels, L.F.A., Van De Vijver, M.J. and Tuschl, T. (2011) MicroRNA Sequence and Expression Analysis in Breast Tumors by Deep Sequencing. Cancer Research, 71, 4443-4453.
[7] Kuballa, P. and Xavier, P.J. (2010) Failure and Exploitation of Autophagy in Human Pathologies—Cellular Integrity between Inflammation, Infection, and Cell Survival. Seminars in Immunopathology, 32, 319-322.
[8] Cai, Z., Zhao, B. and Ratka, A. (2011) Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease. NeuroMo-lecular Medicine, 13, 223-250.
[9] Klionsky, D.J. (2008) Autophagy Revisited: A Conversation with Christian de Duve. Autophagy, 4, 740-743.
[10] Wang, C.W. and Klionsky, D.J. (2003) The Molecular Mechanism of Autophagy. Molecular Medicine, 9, 65-76.
[11] Mienincn, T.A., Railo, M., Lepntalo, M., et al. (2005) Plant Sterols in Serum and in Atherosclerotic Plaques of Patients Undergoing Carotid Endarterectomy. Journal of the American College of Cardiology, 45, 1794-1801.
[12] Chau, Y.P., Lin, S.Y., Chen, J.H., et al. (2003) Endostatin Induces Autophagic Cell Death Endothelial Cells. Histology and Histopathology, 18, 715-726.
[13] Nowicki, M., Zabirnyk, O., Duerrschmidt, N., et al. (2007) NO Upregulation of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 in Serumdeprived EA. hy926 Human Endothelial Cells under Oxldl Exposure, but Increase in Autophagy. European Journal of Cell Biology, 86, 605-616.
[14] Kockx, M.M., De Meyer, G.R., Buyssens, N., et al. (1998) Cell Composition, Replication, and Apoptosis and in Atherosclerotic Plaques after 6 Months of Cholesterol Withdrawal. Circulation Research, 83, 378-387.
[15] Kockx, M.M., De Meyer, G.R., Buyssens, N., et al. (1998) Apoptosisd and Related Proteins in Different Stages of Human Atherosclerotic Plaques. Circulation, 97, 2307-2315.
[16] Gui, T., Shimokado, Sun, Y., et al. (2012) Diverse Roles of Macrophages in Atherosclerosis: From Inflammatory Biology to Biomarker Discovery. Mediators of Inflammation, 2012, Article ID: 693083.
[17] Matsuzawa, T., Kim, B.H., Shenoy, A.R., et al. (2012) IFN-r Elicits Macrophage Autophagy via the p38 MAPK Sig-naling Pathway. The Journal of Immunology, 189, 813-818.
[Google Scholar] [CrossRef] [PubMed]
[18] Razani, B., Feng, C., Coleman, T., et al. (2012) Autophagy Links Inflammasomes to Atherosclerotic Progression. Cell Metabolism, 15, 534-544.
[Google Scholar] [CrossRef] [PubMed]
[19] Huang, H.P., Li, X.Y., Zhang, Y., et al. (2014) Class A Scavenger Receptor Activation Inhibits Endoplasmic Reticulum Stress-Induced Autophagy in Macrophage. Journal of Biomedical Research, 28, 213-221.
[20] Yen, W.L., Legakis, J.E., Nair, U. and Klionsky, D.J. (2007) Atg27 Is Required for Autophagy-Dependent Cycling of Atg9. Molecular Biology of the Cell, 18, 581-593.
[21] Hailey, D.W., Rambold, A.S., Satpute-Krishnan, P., Mitra, K., Sougrat, R., Kim, P.K. and Lippincott-Schwartz, J. (2010) Mitochondria Supply Membranes for Autophagosome Biogenesis during Starvation. Cell, 141, 656-667.

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