Qianhui Xu, Huilan Wang, Ruonan Yang, Youqi Tao, Ziying Wang, Shengnan Zhang, Bo Sun, Dan Li, Boxun Lu, Cong Liu
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引用次数: 0
Abstract
Dear Editor,
Parkinson’s disease (PD) is a progressive neurodegenerative disorder, which manifests through the abnormal accumulation of pathological amyloid fibrils composed of α-synuclein (α-syn) into Lewy bodies and the deterioration of dopaminergic neurons in the substantia nigra.1,2,3,4 In addition to α-syn fibrillar aggregation, the disruption of selective autophagy is also tightly linked to the pathogenesis of PD.5,6 The co-localization of LC3B, the key autophagosome protein in selective autophagy,7 and α-syn in the Lewy bodies of PD patients’ brains points towards a potential role of α-syn in modulating selective autophagy.8 Yet, the interplay between them has not been mechanistically elucidated.
期刊介绍：
Cell Research (CR) is an international journal published by Springer Nature in partnership with the Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences (CAS). It focuses on publishing original research articles and reviews in various areas of life sciences, particularly those related to molecular and cell biology. The journal covers a broad range of topics including cell growth, differentiation, and apoptosis; signal transduction; stem cell biology and development; chromatin, epigenetics, and transcription; RNA biology; structural and molecular biology; cancer biology and metabolism; immunity and molecular pathogenesis; molecular and cellular neuroscience; plant molecular and cell biology; and omics, system biology, and synthetic biology. CR is recognized as China's best international journal in life sciences and is part of Springer Nature's prestigious family of Molecular Cell Biology journals.
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