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细胞骨架失调与神经退行性疾病:丝切蛋白 - 肌动蛋白杆的形成、监测及抑制

Cytoskeletal dysregulation and neurodegenerative disease: Formation, monitoring, and inhibition of cofilin-actin rods.

作者信息

Wurz Anna I, Schulz Anna M, O'Bryant Collin T, Sharp Josephine F, Hughes Robert M

机构信息

Department of Chemistry, East Carolina University, Greenville, NC, United States.

Department of Chemistry, Notre Dame College, South Euclid, OH, United States.

出版信息

Front Cell Neurosci. 2022 Sep 22;16:982074. doi: 10.3389/fncel.2022.982074. eCollection 2022.

DOI:10.3389/fncel.2022.982074
PMID:36212686
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9535683/
Abstract

The presence of atypical cytoskeletal dynamics, structures, and associated morphologies is a common theme uniting numerous diseases and developmental disorders. In particular, cytoskeletal dysregulation is a common cellular feature of Alzheimer's disease, Parkinson's disease, and Huntington's disease. While the numerous activators and inhibitors of dysregulation present complexities for characterizing these elements as byproducts or initiators of the disease state, it is increasingly clear that a better understanding of these anomalies is critical for advancing the state of knowledge and plan of therapeutic attack. In this review, we focus on the hallmarks of cytoskeletal dysregulation that are associated with cofilin-linked actin regulation, with a particular emphasis on the formation, monitoring, and inhibition of cofilin-actin rods. We also review actin-associated proteins other than cofilin with links to cytoskeleton-associated neurodegenerative processes, recognizing that cofilin-actin rods comprise one strand of a vast web of interactions that occur as a result of cytoskeletal dysregulation. Our aim is to present a current perspective on cytoskeletal dysregulation, connecting recent developments in our understanding with emerging strategies for biosensing and biomimicry that will help shape future directions of the field.

摘要

非典型细胞骨架动力学、结构及相关形态的存在是众多疾病和发育障碍的一个共同主题。特别是,细胞骨架失调是阿尔茨海默病、帕金森病和亨廷顿病常见的细胞特征。虽然失调的众多激活剂和抑制剂使得将这些因素表征为疾病状态的副产品或引发剂变得复杂,但越来越明显的是,更好地理解这些异常对于推进知识水平和治疗策略至关重要。在本综述中,我们聚焦于与丝切蛋白相关的肌动蛋白调节相关的细胞骨架失调特征,特别强调丝切蛋白 - 肌动蛋白杆的形成、监测和抑制。我们还综述了除丝切蛋白外与细胞骨架相关神经退行性过程有关的肌动蛋白相关蛋白,认识到丝切蛋白 - 肌动蛋白杆是细胞骨架失调导致的大量相互作用网络中的一条线索。我们的目的是呈现细胞骨架失调的当前观点,将我们理解中的最新进展与生物传感和仿生学的新兴策略联系起来,这将有助于塑造该领域的未来方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d6/9535683/7d8cea83cd82/fncel-16-982074-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d6/9535683/8936bfb790e6/fncel-16-982074-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d6/9535683/b7886c01a2c9/fncel-16-982074-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d6/9535683/69b868c80271/fncel-16-982074-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d6/9535683/7d8cea83cd82/fncel-16-982074-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d6/9535683/8936bfb790e6/fncel-16-982074-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d6/9535683/b7886c01a2c9/fncel-16-982074-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d6/9535683/69b868c80271/fncel-16-982074-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d6/9535683/7d8cea83cd82/fncel-16-982074-g004.jpg

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