自噬
神经保护
神经退行性变
未折叠蛋白反应
氧化应激
串扰
细胞生物学
内质网
神经科学
生物
化学
疾病
医学
生物化学
细胞凋亡
病理
物理
光学
作者
Yasaman Esmaeili,Zahra Yarjanli,Fatemeh Paknia,Elham Bidram,Marek Łos,Mehdi Eshraghi,Daniel J. Klionsky,Saeid Ghavami,Ali Zarrabi
标识
DOI:10.1016/j.jconrel.2022.03.001
摘要
Protein homeostasis is a vital process for cell function and, therefore, disruption of the molecular mechanisms involved in this process, such as autophagy, may contribute to neurodegenerative diseases (NDs). Apart from autophagy disruption, excess oxidative stress and endoplasmic reticulum (ER) stress are additional main molecular mechanisms underlying neurodegeneration, leading to protein aggregation, and mitochondrial dysfunction. Notably, these primary molecular processes are interconnected pathways, which have synergistic effects on each other. Therefore, we propose that targeting of the crosstalk between autophagy, oxidative stress and ER stress simultaneously may play a critical role in healing NDs. NeuroNanoTechnology, as a revolutionized approach, in combination with an in-silico strategy, holds great promise for developing de-novo structures for targeting and modulating neuro-molecular pathways. Accordingly, this review outlines the contributions of autophagy, oxidative stress, and ER stress in neurodegenerative conditions along with a particular focus on the crosstalk among these pathways. Furthermore, we provide a comprehensive discussion on the potential of nanomaterials to target this crosstalk and suggest this potential as a promising opportunity in neuroprotection.
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