Mitochondrial-based therapies for neurodegenerative diseases: a review of the current literature.

IF 3.1 4区 医学 Q2 PHARMACOLOGY & PHARMACY Naunyn-Schmiedeberg's archives of pharmacology Pub Date : 2025-09-01 Epub Date: 2025-03-31 DOI:10.1007/s00210-025-04014-0
Al-Hassan Soliman Wadan, Ahmed H Shaaban, Mohamed Z El-Sadek, Salah Abdelfatah Mostafa, Ahmed Sherief Moshref, Ahmed El-Hussein, Doha El-Sayed Ellakwa, Samah S Mehanny
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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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基于线粒体的神经退行性疾病疗法:当前文献综述。
神经退行性疾病由于其复杂的病因、发病机制和进行性,使实际治疗方法复杂化,对现代医学提出了重大挑战。线粒体功能障碍是各种神经退行性疾病的病理生理学的重要贡献者,包括阿尔茨海默病(AD)、帕金森病(PD)和肌萎缩侧索硬化症(ALS)。本文回顾了目前的文献,重点介绍了线粒体的多方面功能,包括能量产生、钙信号传导、细胞凋亡调节、线粒体生物发生、线粒体动力学、轴突运输、内质网-线粒体相互作用、线粒体自噬、线粒体蛋白质平衡以及它们在神经元健康中的重要作用。文献强调,越来越多的人认识到线粒体功能障碍是神经退行性疾病进展的关键因素,标志着从传统的症状管理到创新的线粒体治疗的转变。通过讨论线粒体机制,包括线粒体质量控制(MQC)过程和氧化应激的影响,本综述强调需要新的治疗策略来恢复线粒体功能,保护神经元连接和完整性,并减缓疾病进展。这篇全面的综述旨在为潜在的干预措施提供见解,这些干预措施可以改变神经退行性疾病的治疗前景,解决症状和潜在的病理生理变化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
6.20
自引率
5.60%
发文量
142
审稿时长
4-8 weeks
期刊介绍: Naunyn-Schmiedeberg''s Archives of Pharmacology was founded in 1873 by B. Naunyn, O. Schmiedeberg and E. Klebs as Archiv für experimentelle Pathologie und Pharmakologie, is the offical journal of the German Society of Experimental and Clinical Pharmacology and Toxicology (Deutsche Gesellschaft für experimentelle und klinische Pharmakologie und Toxikologie, DGPT) and the Sphingolipid Club. The journal publishes invited reviews, original articles, short communications and meeting reports and appears monthly. Naunyn-Schmiedeberg''s Archives of Pharmacology welcomes manuscripts for consideration of publication that report new and significant information on drug action and toxicity of chemical compounds. Thus, its scope covers all fields of experimental and clinical pharmacology as well as toxicology and includes studies in the fields of neuropharmacology and cardiovascular pharmacology as well as those describing drug actions at the cellular, biochemical and molecular levels. Moreover, submission of clinical trials with healthy volunteers or patients is encouraged. Short communications provide a means for rapid publication of significant findings of current interest that represent a conceptual advance in the field.
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