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The Emerging Roles of Ferroptosis in Huntington's Disease
Yajing Mi1, Xingchun Gao1, Hao Xu1
1Shaanxi Key Laboratory of Brain Disorders, and Department of Basic Medicine, Xi'an Medical University, Xi'an, 710021, China.
Insights
Huntington's disease (HD) involves iron-dependent cell death called ferroptosis. Inhibiting ferroptosis may offer new therapeutic strategies for this neurodegenerative disorder.
Area of Science:
- Neuroscience
- Genetics
- Cell Biology
Background:
- Huntington's disease (HD) is a fatal neurodegenerative disorder with a known genetic cause (abnormal CAG repeat in the huntingtin gene).
- The precise molecular mechanisms driving neuronal death in HD remain unclear, limiting effective treatment options.
- Ferroptosis, a form of iron-dependent cell death, is increasingly implicated in neurodegenerative diseases.
Purpose of the Study:
- To review the evidence linking ferroptosis to Huntington's disease.
- To summarize the molecular mechanisms of ferroptosis in HD.
- To outline potential therapeutic strategies targeting ferroptosis for HD.
Main Methods:
- Review of existing literature on ferroptosis and Huntington's disease.
- Analysis of data from human patients and mouse models of HD.
- Synthesis of current understanding of ferroptosis pathways in neurodegeneration.
Main Results:
- Strong evidence suggests a significant role for ferroptosis in the pathology of Huntington's disease.
- Specific molecules and signaling pathways involved in ferroptosis contribute to neuronal death in HD.
- Inhibiting ferroptosis has shown promise in alleviating HD symptoms and pathology in preclinical studies.
Conclusions:
- Ferroptosis is a key cellular process implicated in Huntington's disease progression.
- Targeting ferroptosis pathways presents a promising therapeutic avenue for HD.
- Further research into ferroptosis mechanisms in HD could lead to novel treatments.
Abstract:
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.