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DOI 10.1016/j.cellsig.2025.111715

Медицинская библиотека · Cellular signalling · 2025

Neurodegenerative diseases: Epigenetic regulatory mechanisms and therapeutic potential.

Men Jianbing, Wang Xinyue, Zhou Yunnuo, Huang Yumeng, Zheng Yue, Wang Yingze, Yang Shuang, Chen Nan, Yan Nan, Duan Xiaoxu

СтатьяОбзорПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

Neurodegenerative diseases (NDDs) are a class of diseases in which the progressive loss of subtype-specific neurons leads to dysfunction. NDDs include Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS), among others. Previous studies have demonstrated that the pathogenesis of NDDs involves various mechanisms, including genetic factors, oxidative stress, apoptosis, and the immune response. Recent studies have shown that epigenetic regulation mediates the interactions between DNA methylation, chromatin remodeling, histone modification, and non-coding RNAs, thus affecting gene transcription. A growing body of research links epigenetic modifications to crucial pathways involved in the occurrence and development of NDDs. Epigenetics has also been found to regulate and maintain nervous system function, and its imbalance is closely related to the occurrence and development of NDDs. The present review summarizes focuses on the role of epigenetic modifications in the pathogenesis of NDDs and provides an overview of the key genes regulated by DNA methylation, histone modification, and non-coding RNAs in NDDs. Further, the current research status of epigenetics in NDDs is summarized and the potential application of epigenetics in the clinical diagnosis and treatment of NDDs is discussed.

Для цитирования: Men Jianbing, Wang Xinyue, Zhou Yunnuo, Huang Yumeng, Zheng Yue, Wang Yingze, Yang Shuang, Chen Nan, Yan Nan, Duan Xiaoxu. Neurodegenerative diseases: Epigenetic regulatory mechanisms and therapeutic potential.. Cellular signalling. 2025. DOI: 10.1016/j.cellsig.2025.111715.

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