铁死亡在帕金森病中的研究进展

张春莉; 李红燕

doi:10.16766/j.cnki.issn.1674-4152.003888

铁死亡在帕金森病中的研究进展

doi: 10.16766/j.cnki.issn.1674-4152.003888

张春莉¹,
李红燕^2, ,

1.
新疆维吾尔自治区人民医院神经内科，新疆乌鲁木齐 830000
2.
新疆脑卒中与神经系统罕见病临床医学研究中心，新疆乌鲁木齐 830000

基金项目:

国家自然科学基金地区科学基金项目 31560270

详细信息

通讯作者:
李红燕，E-mail：lhyxxy_008@126.com

中图分类号: R742.5
计量
- 文章访问数: 11
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- PDF下载量: 1
- 被引次数: 0
出版历程
- 收稿日期: 2024-02-20
- 网络出版日期: 2025-03-27

Research progress on iron death in Parkinson ' s disease

ZHANG Chunli¹,
LI Hongyan^{2
, ,}

1.
Department of Neurology, Xinjiang Uygur Autonomous Region People ' s Hospital, Urumqi, Xinjiang 830000, China

摘要

摘要: 帕金森病(PD)是一种年龄依赖性、迟发性神经退行性疾病，主要以典型的运动症状及非运动症状为特征。目前PD的病因、机制尚不完全清楚，但除了传统观点认为的黑质致密部多巴胺能神经元的退化，以及其细胞内α-突触核蛋白异常沉积外，人们逐渐发现多种新型细胞死亡方式参与了PD的发展过程，其中包括细胞焦亡、细胞自噬和细胞铁死亡。细胞铁死亡作为一种新型程序性细胞死亡方式，是由脂质过氧化过度驱动和铁依赖性调节，其与PD在病理生理学上有共同特点。细胞铁死亡主要是由铁过度沉积、氨基酸代谢失衡、脂质过氧化和线粒体损伤等导致神经细胞毒性，最终导致神经元细胞死亡和丧失。因此，铁螯合剂、铁死亡抑制剂和亲脂抗氧化剂等一些相关药物可以通过抑制金属离子反应，减少铁代谢失衡和氧化应激损伤来抑制细胞铁死亡，从而干预PD的发病和进展。基于此，本文针对铁死亡在PD中的潜在致病机制及选择性抑制细胞铁死亡在缓解和治疗PD中的分子机理进行总结，为进一步开发靶向抑制铁死亡的干预和治疗PD奠定了基础。同时研究细胞铁死亡的机制可以为未来的药物研发提供新的思路和方向，以帮助改善PD患者的生活质量，延缓疾病的进展，为PD的治疗和管理提供更多的可能性。
- 帕金森病 /
- 铁死亡 /
- 铁代谢 /
- 脂质过氧化 /
- 铁死亡抑制剂 /
- 亲脂抗氧化剂
Abstract: Parkinson ' s disease (PD) is an age-dependent late-onset neurodegenerative disorder characterized by classic motor and non-motor symptoms. At present, the etiology and mechanism of PD are not fully understood, but in addition to the degeneration of dopaminergic neurons in the substantia nigra densa and the abnormal deposition of α-synuclein in their cells, it has been gradually discovered that a variety of new cell death modes are involved in the development of PD, including pyroptosis, autophagy, and iron death. Cell iron death, as a new type of programmed cell death, is overdriven by lipid peroxidation and regulated by iron dependence, which has common pathophysiological features with PD. Cellular iron death is mainly caused by excessive iron deposition, imbalance of amino acid metabolism, lipid peroxidation, and mitochondrial damage, which lead to nerve cell toxicity, and eventually lead to neuronal cell death and loss. Therefore, some related drugs, such as iron chelating agents, iron death inhibitors, and lipophilic antioxidants, can inhibit cell iron death by inhibiting metal ion reaction, reducing iron metabolism imbalance and oxidative stress damage, so as to intervene in the pathogenesis and progression of PD. Based on this, this paper summarized the potential pathogenic mechanism of iron death in PD and the molecular mechanism of selective inhibition of cell iron death in the remission and treatment of PD, laying a foundation for further development of targeted intervention and treatment of iron death. At the same time, studying the mechanism of cell iron death can provide new ideas and directions for future drug development, help improve the quality of life of PD patients, delay the progression of the disease, and provide more possibilities for the treatment and management of PD.
- Parkinson ' s disease /
- Iron death /
- Iron metabolism /
- Lipid peroxidation /
- Iron death inhibitor /
- Lipophilic antioxidant

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参考文献(42)

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