神经退行性变
神经科学
肌萎缩侧索硬化
生物
线粒体
细胞器
帕金森病
疾病
舱室(船)
细胞生物学
医学
病理
海洋学
地质学
作者
Shivkumar S. Sammeta,Trupti A. Banarase,Sandip R. Rahangdale,Nitu L. Wankhede,Manish M. Aglawe,Brijesh G. Taksande,Shubhada V. Mangrulkar,Aman Upaganlawar,Sushruta Koppula,Spandana Rajendra Kopalli,Milind J. Umekar,Mayur B. Kale
标识
DOI:10.1016/j.mito.2023.07.005
摘要
Biological researchers are seeing organelles in a new light. These cellular entities have been believed to be singular and distinctive structures that performed specialized purposes for a very long time. But in recent past years, scientists have learned that organelles become dynamic and make physical contact. Additionally, Biological processes are regulated by organelles interactions and its alteration play an important role in cell malfunctioning and several pathologies, including neurodegenerative diseases. Mitochondrial-ER contact sites (MERCS) have received considerable attention in the domain of cell homeostasis and dysfunction, specifically in the area of neurodegeneration. This is largely due to the significant role of this subcellular compartment in a diverse array of vital cellular functions, including Ca2+ homeostasis, transport, bioenergetics and turnover, mitochondrial dynamics, apoptotic signaling, ER stress, and inflammation. A significant number of disease-associated proteins were found to physically interact with the ER-Mitochondria (ER-MT) interface, causing structural and/or functional alterations in this compartment. In this review, we summarize current knowledge about the structure and functions of the ER-MT contact sites, as well as the possible repercussions of their alteration in notable neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and fronto-temporal dementia. The constraints and complexities in defining the nature and origin of the highlighted defects in ER-MT communication, as well as their concise contribution to the neurodegenerative process, are illustrated in particular. The possibility of using MERCS as a potential drug target to prevent neuronal damage and ultimately neurodegeneration is the topic of our final discussion.
科研通智能强力驱动
Strongly Powered by AbleSci AI