PDF(Pubmed)
Abstract：
Chronic neuroinflammation serves a key role in the onset and progression of neurodegenerative disorders. Mitochondria serve as central regulators of neuroinflammation. In addition to providing energy to cells, mitochondria also participate in the immunoinflammatory response of neurodegenerative disorders including Alzheimer\'s disease, Parkinson\'s disease, multiple sclerosis and epilepsy, by regulating processes such as cell death and inflammasome activation. Under inflammatory conditions, mitochondrial oxidative stress, epigenetics, mitochondrial dynamics and calcium homeostasis imbalance may serve as underlying regulatory mechanisms for these diseases. Therefore, investigating mechanisms related to mitochondrial dysfunction may result in therapeutic strategies against chronic neuroinflammation and neurodegeneration. The present review summarizes the mechanisms of mitochondria in chronic neuroinflammatory diseases and the current treatment approaches that target mitochondrial dysfunction in these diseases.
摘要：
慢性神经炎症在神经退行性疾病的发生和发展中起关键作用。线粒体作为神经炎症的中枢调节因子。除了为细胞提供能量，线粒体也参与包括阿尔茨海默病在内的神经退行性疾病的免疫炎症反应，帕金森病,多发性硬化症和癫痫，通过调节细胞死亡和炎性体激活等过程。在炎症条件下，线粒体氧化应激，表观遗传学,线粒体动力学和钙稳态失衡可能是这些疾病的潜在调节机制.因此,研究与线粒体功能障碍相关的机制可能会导致针对慢性神经炎症和神经变性的治疗策略。本文综述了线粒体在慢性神经炎性疾病中的作用机制以及目前针对这些疾病中线粒体功能障碍的治疗方法。
