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      Cell death and inflammation during obesity: “Know my methods, WAT(son)”

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          Abstract

          Obesity is a state of low-grade chronic inflammation that causes multiple metabolic diseases. During obesity, signalling via cytokines of the TNF family mediate cell death and inflammation within the adipose tissue, eventually resulting in lipid spill-over, glucotoxicity and insulin resistance. These events ultimately lead to ectopic lipid deposition, glucose intolerance and other metabolic complications with life-threatening consequences. Here we review the literature on how inflammatory responses affect metabolic processes such as energy homeostasis and insulin signalling. This review mainly focuses on the role of cell death in the adipose tissue as a key player in metabolic inflammation.

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          AMPK: guardian of metabolism and mitochondrial homeostasis.

          Sébastien Herzig, Reuben Shaw (2018)
          Cells constantly adapt their metabolism to meet their energy needs and respond to nutrient availability. Eukaryotes have evolved a very sophisticated system to sense low cellular ATP levels via the serine/threonine kinase AMP-activated protein kinase (AMPK) complex. Under conditions of low energy, AMPK phosphorylates specific enzymes and growth control nodes to increase ATP generation and decrease ATP consumption. In the past decade, the discovery of numerous new AMPK substrates has led to a more complete understanding of the minimal number of steps required to reprogramme cellular metabolism from anabolism to catabolism. This energy switch controls cell growth and several other cellular processes, including lipid and glucose metabolism and autophagy. Recent studies have revealed that one ancestral function of AMPK is to promote mitochondrial health, and multiple newly discovered targets of AMPK are involved in various aspects of mitochondrial homeostasis, including mitophagy. This Review discusses how AMPK functions as a central mediator of the cellular response to energetic stress and mitochondrial insults and coordinates multiple features of autophagy and mitochondrial biology.
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            Mechanisms and functions of inflammasomes.

            Mohamed Lamkanfi, Vishva Dixit (2014)
            Recent studies have offered a glimpse into the sophisticated mechanisms by which inflammasomes respond to danger and promote secretion of interleukin (IL)-1β and IL-18. Activation of caspases 1 and 11 in canonical and noncanonical inflammasomes, respectively, also protects against infection by triggering pyroptosis, a proinflammatory and lytic mode of cell death. The therapeutic potential of inhibiting these proinflammatory caspases in infectious and autoimmune diseases is raised by the successful deployment of anti-IL-1 therapies to control autoinflammatory diseases associated with aberrant inflammasome signaling. This Review summarizes recent insights into inflammasome biology and discusses the questions that remain in the field. Copyright © 2014 Elsevier Inc. All rights reserved.
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              Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase.

              Liming Sun, Huayi Wang, Zhigao Wang … (2012)
              The receptor-interacting serine-threonine kinase 3 (RIP3) is a key signaling molecule in the programmed necrosis (necroptosis) pathway. This pathway plays important roles in a variety of physiological and pathological conditions, including development, tissue damage response, and antiviral immunity. Here, we report the identification of a small molecule called (E)-N-(4-(N-(3-methoxypyrazin-2-yl)sulfamoyl)phenyl)-3-(5-nitrothiophene-2-yl)acrylamide--hereafter referred to as necrosulfonamide--that specifically blocks necrosis downstream of RIP3 activation. An affinity probe derived from necrosulfonamide and coimmunoprecipitation using anti-RIP3 antibodies both identified the mixed lineage kinase domain-like protein (MLKL) as the interacting target. MLKL was phosphorylated by RIP3 at the threonine 357 and serine 358 residues, and these phosphorylation events were critical for necrosis. Treating cells with necrosulfonamide or knocking down MLKL expression arrested necrosis at a specific step at which RIP3 formed discrete punctae in cells. These findings implicate MLKL as a key mediator of necrosis signaling downstream of the kinase RIP3. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Nieves Peltzer:
                ORCID: http://orcid.org/0000-0002-4134-5852
                m.peltzer@uni-koeln.de
                Journal
                Journal ID (nlm-ta): Cell Death Differ
                Journal ID (iso-abbrev): Cell Death Differ
                Title: Cell Death and Differentiation
                Publisher: Nature Publishing Group UK (London )
                ISSN (Print): 1350-9047
                ISSN (Electronic): 1476-5403
                Publication date (Electronic): 29 September 2022
                Publication date PMC-release: 29 September 2022
                Pages: 1-14
                Affiliations
                GRID grid.6190.e, ISNI 0000 0000 8580 3777, University of Cologne, Faculty of Medicine, Centre for Molecular Medicine Cologne (CMMC); Department of Translational Genomics and; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), ; Cologne, Germany
                Author information
                http://orcid.org/0000-0002-4134-5852
                Article
                Publisher ID: 1062
                DOI: 10.1038/s41418-022-01062-4
                PMC ID: 9520110
                PubMed ID: 36175539
                SO-VID: d40fb1be-493c-430c-90be-8156e25439aa
                Copyright © © The Author(s) 2022
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 25 May 2022
                Date revision received : 8 September 2022
                Date accepted : 9 September 2022
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100001659, Deutsche Forschungsgemeinschaft (German Research Foundation);
                Award ID: 413326622
                Award ID: 414786233
                Award ID: 455784452
                Award Recipient :
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Cell biology
                Keywords: ageing,cell death and immune response,chronic inflammation
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: ageing, cell death and immune response, chronic inflammation

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