The Emerging Roles of Ferroptosis in Huntington’s Disease

  • Yajing Mi
  • Xingchun Gao
  • Hao Xu
  • Yuanyuan Cui
  • Yuelin ZhangEmail author
  • Xingchun GouEmail author
Review Paper


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.


Huntington’s disease Ferroptosis Mutant Huntingtin Lipid peroxidation Iron accumulation 



This work was supported by National Natural Science Foundation of China (81873740, 81471415, 81500063, 31600951, 81801088), Natural Science Basic Research Plan in Shaanxi Province of China (2017JM8086, 2017JQ8048), The Leading Disciplines Development Government Foundation of Shaanxi, and Xi’an Medical University’s key disciplines of molecular immunology.

Compliance with Ethical Standards

Conflict of interest

The authors declare no conflict of interest.


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Authors and Affiliations

  1. 1.Shaanxi Key Laboratory of Brain Disorders, and Department of Basic MedicineXi’an Medical UniversityXi’anChina

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