线粒体
炎症体
线粒体生物发生
神经退行性变
疾病
神经科学
生物
生物发生
细胞生物学
医学
免疫学
遗传学
炎症
病理
基因
作者
Joseph Johnson,Elizabeth Mercado‐Ayón,Yesica Mercado-Ayon,Yi Dong,Sarah Halawani,Lucie Vanessa Ngaba,David R. Lynch
标识
DOI:10.1016/j.abb.2020.108698
摘要
In addition to ATP synthesis, mitochondria are highly dynamic organelles that modulate apoptosis, ferroptosis, and inflammasome activation. Through executing these varied functions, the mitochondria play critical roles in the development and progression of neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and Friedreich ataxia, among others. Impaired mitochondrial biogenesis and abnormal mitochondrial dynamics contribute to mitochondrial dysfunction in these diseases. Additionally, dysfunctional mitochondria play critical roles in signaling for both inflammasome activation and ferroptosis. Therapeutics are being developed to circumvent inflammasome activation and ferroptosis in dysfunctional mitochondria. Targeting these aspects of mitochondrial dysfunction may present viable therapeutic strategies for combatting the neurodegenerative diseases. This review aims to summarize the role of the mitochondria in the development and progression of neurodegenerative diseases and to present current therapeutic approaches that target mitochondrial dysfunction in these diseases.
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