Journal
NEUROMOLECULAR MEDICINE
Volume 21, Issue 2, Pages 110-119Publisher
HUMANA PRESS INC
DOI: 10.1007/s12017-018-8518-6
Keywords
Huntington's disease; Ferroptosis; Mutant Huntingtin; Lipid peroxidation; Iron accumulation
Categories
Funding
- National Natural Science Foundation of China [81873740, 81471415, 81500063, 31600951, 81801088]
- Natural Science Basic Research Plan in Shaanxi Province of China [2017JM8086, 2017JQ8048]
- Leading Disciplines Development Government Foundation of Shaanxi
- Xi'an Medical University's key disciplines of molecular immunology
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Huntington's disease (HD) is an autosomal dominant and fatal neurodegenerative disorder, which is caused by an abnormal CAG repeat in the huntingtin gene. Despite its well-defined genetic origin, the molecular mechanisms of neuronal death are unclear yet, thus there are no effective strategies to block or postpone the process of HD. Ferroptosis, a recently identified iron-dependent cell death, attracts considerable attention due to its putative involvement in neurodegenerative diseases. Accumulative data suggest that ferroptosis is very likely to participate in HD, and inhibition of the molecules and signaling pathways involved in ferroptosis can significantly eliminate the symptoms and pathology of HD. This review first describes evidence for the close relevance of ferroptosis and HD in patients and mouse models, then summarizes advances for the mechanisms of ferroptosis involved in HD, finally outlines some therapeutic strategies targeted ferroptosis. Comprehensive understanding of the emerging roles of ferroptosis in the occurrence of HD will help us to explore effective therapies for slowing the progression of this disease.
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