We are analyzing https://link.springer.com/article/10.1007/s00109-019-01795-9.

Title:
AMPK activation inhibits the functions of myeloid-derived suppressor cells (MDSC): impact on cancer and aging | Journal of Molecular Medicine
Description:
AMP-activated protein kinase (AMPK) has a crucial role not only in the regulation of tissue energy metabolism but it can also control immune responses through its cooperation with immune signaling pathways, thus affecting immunometabolism and the functions of immune cells. It is known that AMPK signaling inhibits the activity of the NF-κB system and thus suppresses pro-inflammatory responses. Interestingly, AMPK activation can inhibit several major immune signaling pathways, e.g., the JAK-STAT, NF-κB, C/EBPβ, CHOP, and HIF-1α pathways, which induce the expansion and activation of myeloid-derived suppressor cells (MDSC). MDSCs induce an immunosuppressive microenvironment in tumors and thus allow the escape of tumor cells from immune surveillance. Chronic inflammation has a key role in the expansion and activation of MDSCs in both tumors and inflammatory disorders. The numbers of MDSCs also significantly increase during the aging process concurrently with the immunosenescence associated with chronic low-grade inflammation. Increased fatty acid oxidation and lactate produced by aerobic glycolysis are important immunometabolic enhancers of MDSC functions. However, it seems that AMPK signaling regulates the functions of MDSCs in a context-dependent manner. Currently, the activators of AMPK signaling are promising drug candidates for cancer therapy and possibly for the extension of healthspan and lifespan. We will describe in detail the AMPK-mediated regulation of the signaling pathways controlling the expansion and activation of immunosuppressive MDSCs. We will propose that the beneficial effects mediated by AMPK activation, e.g., in cancers and the aging process, could be induced by the inhibition of MDSC functions.
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Keywords {🔍}

pubmed, mdscs, article, google, scholar, cas, cells, ampk, signaling, activation, central, immune, cancer, suppressor, myeloidderived, cell, immunosuppressive, functions, protein, expression, nfκb, pathways, zhang, tumor, immunol, role, expansion, mice, regulation, stat, tumors, increased, aging, activity, differentiation, kinase, responses, inhibits, pathway, inflammation, function, energy, demonstrated, wang, mdsc, cebpβ, mol, metabolism, fatty, immunity,

Topics {✒️}

oxidized low-density lipoprotein amp-activated protein kinase granulocyte-macrophage colony-stimulating factor mir-1a-3p/grp94 pathway ccaat-enhancer-binding protein β ccaat/enhancer-binding protein β nf-κb-dependent signaling induces stabilizes hypoxia-inducible factor-1α orchestrating hif-1α-dependent glycolysis ccaat/enhancer-binding protein revisiting stat3 signalling myeloid-derived suppressor cell myeloid-derived suppressor cells myeloid derived-suppressor cells jak-stat signalling ampk/nf-κb signaling pathway hematopoietic stem cells inf-γ-induced signaling [80] tgf-β-mtor-hif-1 signaling suppresses pro-inflammatory responses pufa-enriched diet augmented hif-1α-dependent glycolytic activity article download pdf myeloid-derived immune cells tgf-β1-activated smad3 hif1α-dependent glycolytic pathway immune-mediated hepatic injury amp kinase sensitive called checkpoint receptors chronic low-grade inflammation immune checkpoint receptor nf-κb signaling pathway mtor-mediated glycolysis contributes triple-negative breast cancer myeloid cell-specific deletion nf-κb-dependent mechanism age-related immune deficiency nf-κb signaling stimulated confers tnf-α resistance jak-stat3 pathway stimulated ampk-dach1-cxcl1 axis mir-185-5p directly targeted c57bl/6j geriatric mice h2o2-induced cardiomyocyte injury tgf-β signaling enhances hypoxia-inducible factor-1α hypoxia-inducible factor 1α jak-stat3 signaling pathway er stress-reducing chaperone nf-κb signaling pathways

Questions {❓}

Bar-Or D, Carrick M, Tanner A 2nd, Lieser MJ, Rael LT, Brody E (2018) Overcoming the Warburg effect: is it the key to survival in sepsis?
Canto C, Auwerx J (2011) Calorie restriction: is AMPK a key sensor and effector?
Hardie DG (2015) Molecular pathways: is AMPK a friend or a foe in cancer?
Liberti MV, Locasale JW (2016) The Warburg effect: how does it benefit cancer cells?
Speirs C, Williams JJL, Riches K, Salt IP, Palmer TM (2018) Linking energy sensing to suppression of JAK-STAT signalling: a potential route for repurposing AMPK activators?
Xu-Monette ZY, Zhang M, Li J, Young KH (2017) PD-1/PD-L1 blockade: have we found the key to unleash the antitumor immune response?

Schema {🗺️}

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         headline:AMPK activation inhibits the functions of myeloid-derived suppressor cells (MDSC): impact on cancer and aging
         description:AMP-activated protein kinase (AMPK) has a crucial role not only in the regulation of tissue energy metabolism but it can also control immune responses through its cooperation with immune signaling pathways, thus affecting immunometabolism and the functions of immune cells. It is known that AMPK signaling inhibits the activity of the NF-κB system and thus suppresses pro-inflammatory responses. Interestingly, AMPK activation can inhibit several major immune signaling pathways, e.g., the JAK-STAT, NF-κB, C/EBPβ, CHOP, and HIF-1α pathways, which induce the expansion and activation of myeloid-derived suppressor cells (MDSC). MDSCs induce an immunosuppressive microenvironment in tumors and thus allow the escape of tumor cells from immune surveillance. Chronic inflammation has a key role in the expansion and activation of MDSCs in both tumors and inflammatory disorders. The numbers of MDSCs also significantly increase during the aging process concurrently with the immunosenescence associated with chronic low-grade inflammation. Increased fatty acid oxidation and lactate produced by aerobic glycolysis are important immunometabolic enhancers of MDSC functions. However, it seems that AMPK signaling regulates the functions of MDSCs in a context-dependent manner. Currently, the activators of AMPK signaling are promising drug candidates for cancer therapy and possibly for the extension of healthspan and lifespan. We will describe in detail the AMPK-mediated regulation of the signaling pathways controlling the expansion and activation of immunosuppressive MDSCs. We will propose that the beneficial effects mediated by AMPK activation, e.g., in cancers and the aging process, could be induced by the inhibition of MDSC functions.
         datePublished:2019-05-25T00:00:00Z
         dateModified:2019-05-25T00:00:00Z
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            Immunosuppression
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            Immunotherapy
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            Trained immunity
            Molecular Medicine
            Human Genetics
            Internal Medicine
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ScholarlyArticle:
      headline:AMPK activation inhibits the functions of myeloid-derived suppressor cells (MDSC): impact on cancer and aging
      description:AMP-activated protein kinase (AMPK) has a crucial role not only in the regulation of tissue energy metabolism but it can also control immune responses through its cooperation with immune signaling pathways, thus affecting immunometabolism and the functions of immune cells. It is known that AMPK signaling inhibits the activity of the NF-κB system and thus suppresses pro-inflammatory responses. Interestingly, AMPK activation can inhibit several major immune signaling pathways, e.g., the JAK-STAT, NF-κB, C/EBPβ, CHOP, and HIF-1α pathways, which induce the expansion and activation of myeloid-derived suppressor cells (MDSC). MDSCs induce an immunosuppressive microenvironment in tumors and thus allow the escape of tumor cells from immune surveillance. Chronic inflammation has a key role in the expansion and activation of MDSCs in both tumors and inflammatory disorders. The numbers of MDSCs also significantly increase during the aging process concurrently with the immunosenescence associated with chronic low-grade inflammation. Increased fatty acid oxidation and lactate produced by aerobic glycolysis are important immunometabolic enhancers of MDSC functions. However, it seems that AMPK signaling regulates the functions of MDSCs in a context-dependent manner. Currently, the activators of AMPK signaling are promising drug candidates for cancer therapy and possibly for the extension of healthspan and lifespan. We will describe in detail the AMPK-mediated regulation of the signaling pathways controlling the expansion and activation of immunosuppressive MDSCs. We will propose that the beneficial effects mediated by AMPK activation, e.g., in cancers and the aging process, could be induced by the inhibition of MDSC functions.
      datePublished:2019-05-25T00:00:00Z
      dateModified:2019-05-25T00:00:00Z
      pageStart:1049
      pageEnd:1064
      sameAs:https://doi.org/10.1007/s00109-019-01795-9
      keywords:
         Aging
         Immunosuppression
         Immunosenescence
         Immunotherapy
         Longevity
         Trained immunity
         Molecular Medicine
         Human Genetics
         Internal Medicine
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         name:Department of Neurology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland
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         name:Department of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland
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            name:University of Eastern Finland
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      name:School of Pharmacy, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland
      name:Department of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland
      name:Department of Ophthalmology, Kuopio University Hospital, Kuopio, Finland

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