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The role of endoplasmic reticulum-mitochondria contact sites in the control of glucose homeostasis: an update
Open accessAbstract
The contact sites that the endoplasmic reticulum (ER) forms with mitochondria, called mitochondria-associated membranes (MAMs), are a hot topic in biological research, and both their molecular determinants and their numerous roles in several signaling pathways are is continuously evolving. MAMs allow the exchange between both organelles of lipids, calcium (Ca 2+), and likely reactive oxygen species, allowing adaptations of both cellular bioenergetics and cell fate depending of cellular needs or stresses. Therefore, it is not surprising that MAMs affect cellular metabolism. Nevertheless, recent arguments suggest that MAMs could also act as key hub of hormonal and/or nutrient signaling in several insulin-sensitive tissues, pointing a specific role of MAMs in the control of glucose homeostasis. Here, I provide a brief review and update on current key signaling roles of the MAMs in the control of glucose homeostasis in both health and metabolic diseases. Particularly, the relevance of ER-mitochondria miscommunication in the disruption of glucose homeostasis is analyzed in details in the liver, skeletal muscle, adipose tissue, and beta cells of the pancreas.
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MAM participate in lipid synthesis, membrane stability, mitochondrial dynamics, and ROS signaling.
“Besides controlling Ca2+ flux, MAM participate in lipid synthesis, membrane stability, mitochondrial dynamics, and ROS signaling [99–101].”
From Neuronal Apolipoprotein E4 Expression Results in Proteome-Wide Alterations and Compromises Bioenergetic Capacity by Disrupting Mitochondrial Function (2019) · cites this paper as [101]
The Inter-organelle signalling section describes lipid synthesis and exchange at MAMs and ROS-mediated signalling. The Metabolic interplay section links MAMs to mitochondrial dynamics. Neither section establishes a role in membrane stability; the paper’s references to MAM integrity concern ER–mitochondria contacts, not membrane stability. Page numbers were unavailable in our copy. (LLM, conf=0.87)
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Metadata
- Authors
- Rieusset, J.
- Affiliations
- Lyon 1 Université (FR)
- Corresponding author
- Rieusset, Jennifer
- ORCID
- Rieusset, Jennifer
- Venue
- Cell Death & Disease
- Published
- 2018-03-09
- Volume
- 9
- Issue
- 3
- Pages
- 388-388
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC5844895
- OpenAlex
- W2792984979
- Cited by
- 248
- References
- 16
- Citations by year
- 2026: 30 · 2025: 25 · 2024: 34 · 2023: 27 · 2022: 25 · 2021: 44 · 2020: 33 · 2019: 20 · 2018: 10
- FWCI
- 2.65
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death and Disease (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondria-associated membranes, ER-mitochondria contact sites, glucose homeostasis, insulin signaling, lipid exchange, calcium exchange, reactive oxygen species, metabolic disorders, liver, skeletal muscle, adipose tissue, pancreatic beta cells, organelle communication
- MeSH terms
- Animals, Calcium, Endoplasmic Reticulum, Glucose, Homeostasis, Humans, Mitochondria
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