摘要
阿尔茨海默病(AD)、帕金森病(PD)、肌萎缩侧索硬化症(ALS)和多发性硬化症等神经退行性疾病(NDD)病变过程中,缺乏能量可能会引起线粒体功能障碍和氧化应激,进一步损害神经元。在炎症条件下,巨噬细胞内的乳酸水平上升,直接作用于组蛋白,引起其乳酸化修饰,促进修复神经元损伤的基因表达。文章就乳酸代谢在神经退行性疾病中的作用机制进行综述,旨在为该类疾病的防治提供新的研究思路。
In the pathological process of neurodegenerative diseases(NDD)such as Alzheimer's disease(AD),Parkinson's disease(PD),amyotrophic lateral sclerosis(ALS)and multiple sclerosis,lack of energy may cause mitochondrial dysfunction and oxi‐dative stress,which further damage neurons.Under inflammatory conditions,the rise of lactate levels in macrophages acted directly on histones,which can cause their lactate modification and promote the expression of genes that repair neuronal damage.This article re‐viewed the mechanism of lactate metabolism in neurodegenerative diseases in order to provide new research ideas for the prevention and treatment of these diseases.
作者
齐正宇(综述)
崔春爱(审校)
QI Zhengyu;CUI Chun'ai(Department of Anatomy,Medical College of Yanbian University,Yanji 133002,Jilin,China)
出处
《医学研究与战创伤救治》
CAS
北大核心
2024年第8期874-878,共5页
Journal of Medical Research & Combat Trauma Care
基金
国家自然科学基金(82060746,81660687)。
关键词
乳酸
乳酸化
神经退行性疾病
翻译后修饰
lactate
lactylation
neurodegenerative diseases
post-translational modification