Journal
NEUROCHEMISTRY INTERNATIONAL
Volume 109, Issue -, Pages 171-183Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2017.03.021
Keywords
ER-mitochondria contacts; Neurodegeneration; Calcium and lipid metabolism; Inflammation; Alzheimer's disease; Parkinson's disease; Amyotrophic lateral sclerosis
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Funding
- Institut national de la sante et de la recherche medicate, Fondation de France [Engt 2012 00034508]
- AETIONOMY (Innovative Medicines Initiative Joint Undertaking, EFPIA companies) [115568]
- Fondation Institut du Cerveau et de la Moelle epiniere
- Agence Nationale de la Recherche (Investissements d'avenir) [ANR-10-IAIHU-06]
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Over the last years, contact sites between the endoplasmic reticulum (ER) and mitochondria have attracted great attention in the study of cell homeostasis and dysfunction, especially in the context of neurodegenerative disorders. This is largely due to the critical involvement of this subcellular compartment in a plethora of vital cellular functions: Ca2+ homeostasis, mitochondrial dynamics, transport, bioenergetics and turnover, ER stress, apoptotic signaling and inflammation. An increasing number of disease-associated proteins have been reported to physically associate with the ER mitochondria interface, and cause structural and/or functional perturbations of this compartment. In the present review, we summarize current knowledge about the architecture and functions of the ER mitochondria contact sites, and the consequences of their alteration in different neurodegenerative disorders. Special emphasis is placed on the caveats and difficulties in defining the nature and origin of the highlighted defects in ER-mitochondria communication, and their exact contribution to the neurodegenerative process. (C) 2017 Elsevier Ltd. All rights reserved.
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