Liu Xiaolei, Huang Sihua, Wang Xingqin, Tang Beisha, Li Wenming, Mao Zixu
Department of Neurology, Xiangya Hospital, Central South University, Changsha, 410008, China.
Neurosci Bull. 2015 Aug;31(4):407-15. doi: 10.1007/s12264-015-1542-8. Epub 2015 Jul 23.
Lysosomes degrade dysfunctional intracellular components via three pathways: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Unlike the other two, CMA degrades cytosolic proteins with a recognized KFERQ-like motif in lysosomes and is important for cellular homeostasis. CMA activity declines with age and is altered in neurodegenerative diseases. Its impairment leads to the accumulation of aggregated proteins, some of which may be directly tied to the pathogenic processes of neurodegenerative diseases. Its induction may accelerate the clearance of pathogenic proteins and promote cell survival, representing a potential therapeutic approach for the treatment of neurodegenerative diseases. In this review, we summarize the current findings on how CMA is involved in neurodegenerative diseases, especially in Parkinson's disease.
巨自噬、微自噬和伴侣介导的自噬(CMA)。与其他两种途径不同,CMA在溶酶体中降解具有公认的类KFERQ基序的胞质蛋白,对细胞内稳态很重要。CMA活性随年龄增长而下降,在神经退行性疾病中也会发生改变。其功能受损会导致聚集蛋白的积累,其中一些可能与神经退行性疾病的致病过程直接相关。诱导CMA可能会加速致病蛋白的清除并促进细胞存活,这代表了一种治疗神经退行性疾病的潜在治疗方法。在这篇综述中,我们总结了目前关于CMA如何参与神经退行性疾病,特别是帕金森病的研究发现。