Crosstalk Between Macroautophagy and Chaperone-Mediated Autophagy: Implications for the Treatment of Neurological Diseases

被引:83
作者
Wu, Haijian [1 ]
Chen, Sheng [1 ]
Ammar, Al-Baadani [1 ]
Xu, Jie [1 ]
Wu, Qun [1 ]
Pan, Kum [2 ]
Zhang, Jianmin [1 ]
Hong, Yuan [1 ]
机构
[1] Zhejiang Univ, Sch Med, Affiliated Hosp 2, Dept Neurosurg, Hangzhou 310003, Zhejiang, Peoples R China
[2] Weill Cornell Med Coll, Dept Neurol Surg, New York, NY USA
基金
高等学校博士学科点专项科研基金; 中国国家自然科学基金;
关键词
Macroautophagy; Chaperone-mediated autophagy; Interplay; Cell biology; Neurological disease; UBIQUITIN-PROTEASOME SYSTEM; ENDOPLASMIC-RETICULUM STRESS; MUTANT ALPHA-SYNUCLEIN; HEAT-SHOCK-PROTEIN; CELL-DEATH; HUNTINGTONS-DISEASE; PARKINSONS-DISEASE; AMYLOID-BETA; MOUSE MODEL; HUMAN BRAIN;
D O I
10.1007/s12035-014-8933-0
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Macroautophagy and chaperone-mediated autophagy (CMA) are two important subtypes of autophagy that play a critical role in cellular quality control under physiological and pathological conditions. Despite the marked differences between these two autophagic pathways, macroautophagy and CMA are intimately connected with each other during the autophagy-lysosomal degradation process, in particular, in the setting of neurological illness. Macroautophagy serves as a backup mechanism to removal of malfunctioning proteins (i.e., aberrant alpha-synuclein) from the cytoplasm when CMA is compromised, and vice versa. The molecular mechanisms underlying the conversation between macroautophagy and CMA are being clarified. Herein, we survey current overviews concentrating on the complex interactions between macroautophagy and CMA, and present therapeutic potentials through utilization and manipulation of macroautophagy-CMA crosstalk in the treatment of neurological diseases.
引用
收藏
页码:1284 / 1296
页数:13
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