线粒体
神经退行性变
自噬
内质网
细胞生物学
氧化应激
帕金森病
未折叠蛋白反应
生物
生物发生
钙信号传导
粒体自噬
神经科学
疾病
信号转导
医学
生物化学
基因
细胞凋亡
病理
作者
Mario Rodríguez‐Arribas,Sokhna M. S. Yakhine-Diop,José Manuel Bravo‐San Pedro,Patricia Gómez‐Suaga,Rubén Gómez‐Sánchez,Guadalupe Martínez-Chacón,José M. Fuentes,Rosa A. González‐Polo,Mireia Niso‐Santano
标识
DOI:10.1007/s12035-016-0140-8
摘要
Mitochondria-associated membranes (MAMs) are structures that regulate physiological functions between endoplasmic reticulum (ER) and mitochondria in order to maintain calcium signaling and mitochondrial biogenesis. Several proteins located in MAMs, including those encoded by PARK genes and some of neurodegeneration-related proteins (huntingtin, presenilin, etc.), ensure this regulation. In this regard, MAM alteration is associated with neurodegenerative diseases such as Parkinson's (PD), Alzheimer's (AD), and Huntington's diseases (HD) and contributes to the appearance of the pathogenesis features, i.e., autophagy dysregulation, mitochondrial dysfunction, oxidative stress, and lately, neuronal death. Moreover,, ER stress and/or damaged mitochondria can be the cause of these disruptions. Therefore, ER-mitochondria contact structure and function are crucial to multiple cellular processes. This review is focused on the molecular interaction between ER and mitochondria indispensable to MAM formation and on MAM alteration-induced etiology of neurodegenerative diseases.
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