Mitochondria-associated membranes (MAMs): An emerging platform connecting energy and immune sensing to metabolic flexibility

被引:23
|
作者
Rieusset, Jennifer [1 ]
机构
[1] Univ Claude Bernard Lyon 1, INRA U1235, INSERM U1060, Lab CarMeN,INSA Lyon, F-69600 Oullins, France
关键词
Organelle communication; Mitochondria-associated membranes; Nutrients; Microbiome; Innate immunity; Insulin sensitivity; Metabolic diseases; ENDOPLASMIC-RETICULUM; MITOFUSIN; 2; INDUCED APOPTOSIS; NUTRIENT AVAILABILITY; REGULATES APOPTOSIS; PROTEOMIC ANALYSIS; CONTACT SITES; ER; DYNAMICS; CALCIUM;
D O I
10.1016/j.bbrc.2017.06.097
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:35 / 44
页数:10
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