ER–mitochondria signaling in Parkinson’s disease

Autor: Rosa A. González-Polo, Patricia Gomez-Suaga, José M. Fuentes, Mireia Niso-Santano, José Manuel Bravo-San Pedro
Přispěvatelé: Institute of Psychiatry, Psychology & Neuroscience, King's College London, King‘s College London, Centre de Recherche des Cordeliers (CRC), Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Gustave Roussy (IGR), Centro de Investigacion Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III [Madrid] (ISC), Universidad de Extremadura (UEX), Université Paris Diderot - Paris 7 (UPD7)-École pratique des hautes études (EPHE)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), CIBER de Enfermedades Neurodegenerativas (CIBERNED)
Jazyk: angličtina
Rok vydání: 2018
Předmět:
Zdroj: Cell Death and Disease, Vol 9, Iss 3, Pp 1-12 (2018)
Cell Death and Disease
Cell Death and Disease, Nature Publishing Group, 2018, 9, pp.337. ⟨10.1038/s41419-017-0079-3⟩
Cell Death & Disease
ISSN: 2041-4889
DOI: 10.1038/s41419-017-0079-3
Popis: Abstract Mitochondria form close physical contacts with a specialized domain of the endoplasmic reticulum (ER), known as the mitochondria-associated membrane (MAM). This association constitutes a key signaling hub to regulate several fundamental cellular processes. Alterations in ER–mitochondria signaling have pleiotropic effects on a variety of intracellular events resulting in mitochondrial damage, Ca2+ dyshomeostasis, ER stress and defects in lipid metabolism and autophagy. Intriguingly, many of these cellular processes are perturbed in neurodegenerative diseases. Furthermore, increasing evidence highlights that ER–mitochondria signaling contributes to these diseases, including Parkinson’s disease (PD). PD is the second most common neurodegenerative disorder, for which effective mechanism-based treatments remain elusive. Several PD-related proteins localize at mitochondria or MAM and have been shown to participate in ER–mitochondria signaling regulation. Likewise, PD-related mutations have been shown to damage this signaling. Could ER–mitochondria associations be the link between pathogenic mechanisms involved in PD, providing a common mechanism? Would this provide a pharmacological target for treating this devastating disease? In this review, we aim to summarize the current knowledge of ER–mitochondria signaling and the recent evidence concerning damage to this signaling in PD.
Databáze: OpenAIRE