粒体自噬
线粒体生物发生
神经科学
蛋白质稳态
线粒体
疾病
肌萎缩侧索硬化
氧化应激
神经退行性变
生物
生物信息学
医学
自噬
细胞生物学
病理
遗传学
细胞凋亡
内分泌学
作者
Al-Hassan Soliman Wadan,Ahmed Shaaban,Mohamed El‐Sadek,S. A. S. Mostafa,Ahmed Sherief Moshref,Ahmed El‐Hussein,Doha El‐Sayed Ellakwa,Samah S Mehanny
标识
DOI:10.1007/s00210-025-04014-0
摘要
Abstract Neurodegenerative disorders present significant challenges to modern medicine because of their complex etiology, pathogenesis, and progressive nature, which complicate practical treatment approaches. Mitochondrial dysfunction is an important contributor to the pathophysiology of various neurodegenerative illnesses, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). This review paper examines the current literature highlighting the multifaceted functions of mitochondria, including energy production, calcium signaling, apoptosis regulation, mitochondrial biogenesis, mitochondrial dynamics, axonal transport, endoplasmic reticulum–mitochondrial interactions, mitophagy, mitochondrial proteostasis, and their crucial involvement in neuronal health. The literature emphasizes the increasing recognition of mitochondrial dysfunction as a critical factor in the progression of neurodegenerative disorders, marking a shift from traditional symptom management to innovative mitochondrial-based therapies. By discussing mitochondrial mechanisms, including mitochondrial quality control (MQC) processes and the impact of oxidative stress, this review highlights the need for novel therapeutic strategies to restore mitochondrial function, protect neuronal connections and integrity, and slow disease progression. This comprehensive review aims to provide insights into potential interventions that could transform the treatment landscape for neurodegenerative diseases, addressing symptoms and underlying pathophysiological changes.
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