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Mediators of Metabolism: An Unconventional Role for NOD1 and NOD2

1
Department of Inflammation & Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 44195, USA
2
Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA
3
Department of Biology, John Carroll University, University Heights, OH 44118, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2021, 22(3), 1156; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031156
Received: 31 December 2020 / Revised: 16 January 2021 / Accepted: 19 January 2021 / Published: 25 January 2021
(This article belongs to the Special Issue The Diversity of Mammalian Nod-Like Receptor Functions)
In addition to their classical roles as bacterial sensors, NOD1 and NOD2 have been implicated as mediators of metabolic disease. Increased expression of NOD1 and/or NOD2 has been reported in a range of human metabolic diseases, including obesity, diabetes, non-alcoholic fatty liver disease, and metabolic syndrome. Although NOD1 and NOD2 share intracellular signaling pathway components, they are differentially upregulated on a cellular level and have opposing impacts on metabolic disease development in mouse models. These NOD-like receptors may directly mediate signaling downstream of cell stressors, such as endoplasmic reticulum stress and calcium influx, or in response to metabolic signals, such as fatty acids and glucose. Other studies suggest that stimulation of NOD1 or NOD2 by their bacterial ligands can result in inflammation, altered insulin responses, increased reactive oxygen signaling, and mitochondrial dysfunction. The activating stimuli for NOD1 and NOD2 in the context of metabolic disease are controversial and may be a combination of both metabolic and circulating bacterial ligands. In this review, we will summarize the current knowledge of how NOD1 and NOD2 may mediate metabolism in health and disease, as well as highlight areas of future investigation. View Full-Text
Keywords: NLR; metabolism; ER stress; mitochondria; hypoxia; high fat diet; metabolic syndrome; insulin resistance; obesity; diabetes NLR; metabolism; ER stress; mitochondria; hypoxia; high fat diet; metabolic syndrome; insulin resistance; obesity; diabetes
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MDPI and ACS Style

Zangara, M.T.; Johnston, I.; Johnson, E.E.; McDonald, C. Mediators of Metabolism: An Unconventional Role for NOD1 and NOD2. Int. J. Mol. Sci. 2021, 22, 1156. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031156

AMA Style

Zangara MT, Johnston I, Johnson EE, McDonald C. Mediators of Metabolism: An Unconventional Role for NOD1 and NOD2. International Journal of Molecular Sciences. 2021; 22(3):1156. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031156

Chicago/Turabian Style

Zangara, Megan T.; Johnston, Isabel; Johnson, Erin E.; McDonald, Christine. 2021. "Mediators of Metabolism: An Unconventional Role for NOD1 and NOD2" Int. J. Mol. Sci. 22, no. 3: 1156. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031156

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