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Lowering Mutant Huntingtin Levels and Toxicity: Autophagy-Endolysosome Pathways in Huntington's Disease

期刊

JOURNAL OF MOLECULAR BIOLOGY
卷 432, 期 8, 页码 2673-2691

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jmb.2019.11.012

关键词

Autophagy; Selective autophagy; Huntington's disease; Huntingtin; Neu rodegeneration

资金

  1. Medical Research Council UK [MR/M023605/1]
  2. UK Academy of Medical Sciences and Newton Fund for Newton Advanced Fellowship [NAF\R1\191045]
  3. National Natural Science Foundation of China [91649105]
  4. MRC [MR/M023605/1] Funding Source: UKRI

向作者/读者索取更多资源

Huntington's disease (HD) is a monogenetic neurodegenerative disease, which serves as a model of neurodegeneration with protein aggregation. Autophagy has been suggested to possess a great value to tackle protein aggregation toxicity and neurodegenerative diseases. Current studies suggest that autophagyendolysosomal pathways are critical for HD pathology. Here we review recent advancement in the studies of autophagy and selective autophagy relating HD. Restoration of autophagy flux and enhancement of selective removal of mutant huntingtin/disease-causing protein would be effective approaches towards tackling HD as well as other similar neurodegenerative disorders. (C) 2019 Elsevier Ltd. All rights reserved.

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