期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 500, 期 1, 页码 35-44出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2017.06.097
关键词
Organelle communication; Mitochondria-associated membranes; Nutrients; Microbiome; Innate immunity; Insulin sensitivity; Metabolic diseases
资金
- recurring funds of INSERM
- National Research Agency [ANR-09-JCJC-0116, ANR-11-BSV1-033-02]
- Fondation pour la recherche medicale [DRM20101220461]
- Servier Laboratories [RPL11002CCA]
- Agence Nationale de la Recherche (ANR) [ANR-09-JCJC-0116] Funding Source: Agence Nationale de la Recherche (ANR)
Living organisms have the capacity to sense both nutrients and immune signals in order to adapt their metabolism to the needs, and both metabolic inflexibility and exacerbated immune responses are associated with metabolic diseases. Over the past decade, mitochondria emerged as key nutrient and immune sensors regulating numerous signalling pathways, and mitochondria dysfunction has been extensively implicated in metabolic diseases. Interestingly, mitochondria interact physically and functionally with the endoplasmic reticulum (ER, in contact sites named mitochondria-associated membranes (MAMs), in order to exchange metabolites and calcium and regulate cellular homeostasis. Emerging evidences suggest that MAMs provide a platform for hormone and nutrient signalling pathways and for innate immune responses, then regulating mitochondrial bioenergetics and apoptosis. Here, I thus propose the concept that MAMs could be attractive nutrient and immune sensors that regulate mitochondria physiology in order to adapt metabolism and cell fate, and that organelle miscommunication could be involved in the metabolic inflexibility and the pro-inflammatory status associated with metabolic diseases. (C) 2017 Elsevier Inc. All rights reserved.
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