Department of Anesthesiology, The Second Affiliated Hospital of Dalian Medical University, Dalian, Liaoning 116000, P.R. China.
Int J Mol Med. 2024 May;53(5). doi: 10.3892/ijmm.2024.5371. Epub 2024 Apr 5.
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.
慢性神经炎症在神经退行性疾病的发病和进展中起着关键作用。线粒体是神经炎症的核心调节者。除了为细胞提供能量外，线粒体还通过调节细胞死亡和炎性小体激活等过程，参与包括阿尔茨海默病、帕金森病、多发性硬化症和癫痫在内的神经退行性疾病的免疫炎症反应。在炎症条件下，线粒体氧化应激、表观遗传学、线粒体动力学和钙动态平衡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产生针对慢性神经炎症和神经退行性变的治疗策略。本综述总结了线粒体在慢性神经炎症性疾病中的作用机制，以及针对这些疾病中线粒体功能障碍的当前治疗方法。
