Готові списки джерел за темами / Metaflammation

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Добірка наукової літератури з теми "Metaflammation"

Автор: Grafiati

Опубліковано: 13 квітня 2024

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Статті в журналах з теми "Metaflammation"

Wei, Lisha, Yan-Yan Zheng, Jie Sun, Pei Wang, Tao Tao, Yeqiong Li, Xin Chen, et al. "GGPP depletion initiates metaflammation through disequilibrating CYB5R3-dependent eicosanoid metabolism." Journal of Biological Chemistry 295, no. 47 (September 10, 2020): 15988–6001. http://dx.doi.org/10.1074/jbc.ra120.015020.

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Metaflammation is a primary inflammatory complication of metabolic disorders characterized by altered production of many inflammatory cytokines, adipokines, and lipid mediators. Whereas multiple inflammation networks have been identified, the mechanisms by which metaflammation is initiated have long been controversial. As the mevalonate pathway (MVA) produces abundant bioactive isoprenoids and abnormal MVA has a phenotypic association with inflammation/immunity, we speculate that isoprenoids from the MVA may provide a causal link between metaflammation and metabolic disorders. Using a line with the MVA isoprenoid producer geranylgeranyl diphosphate synthase (GGPPS) deleted, we find that geranylgeranyl pyrophosphate (GGPP) depletion causes an apparent metaflammation as evidenced by abnormal accumulation of fatty acids, eicosanoid intermediates, and proinflammatory cytokines. We also find that GGPP prenylate cytochrome b5 reductase 3 (CYB5R3) and the prenylated CYB5R3 then translocate from the mitochondrial to the endoplasmic reticulum (ER) pool. As CYB5R3 is a critical NADH-dependent reductase necessary for eicosanoid metabolism in ER, we thus suggest that GGPP-mediated CYB5R3 prenylation is necessary for metabolism. In addition, we observe that pharmacological inhibition of the MVA pathway by simvastatin is sufficient to inhibit CYB5R3 translocation and induces smooth muscle death. Therefore, we conclude that the dysregulation of MVA intermediates is an essential mechanism for metaflammation initiation, in which the imbalanced production of eicosanoid intermediates in the ER serve as an important pathogenic factor. Moreover, the interplay of MVA and eicosanoid metabolism as we reported here illustrates a model for the coordinating regulation among metabolite pathways.

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Embgenbroich, Maria, Hendrik J. P. van der Zande, Leonie Hussaarts, Jonas Schulte-Schrepping, Leonard R. Pelgrom, Noemí García-Tardón, Laura Schlautmann, et al. "Soluble mannose receptor induces proinflammatory macrophage activation and metaflammation." Proceedings of the National Academy of Sciences 118, no. 31 (July 29, 2021): e2103304118. http://dx.doi.org/10.1073/pnas.2103304118.

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Proinflammatory activation of macrophages in metabolic tissues is critically important in the induction of obesity-induced metaflammation. Here, we demonstrate that the soluble mannose receptor (sMR) plays a direct functional role in both macrophage activation and metaflammation. We show that sMR binds CD45 on macrophages and inhibits its phosphatase activity, leading to an Src/Akt/NF-κB–mediated cellular reprogramming toward an inflammatory phenotype both in vitro and in vivo. Remarkably, increased serum sMR levels were observed in obese mice and humans and directly correlated with body weight. Importantly, enhanced sMR levels increase serum proinflammatory cytokines, activate tissue macrophages, and promote insulin resistance. Altogether, our results reveal sMR as regulator of proinflammatory macrophage activation, which could constitute a therapeutic target for metaflammation and other hyperinflammatory diseases.

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Hotamisligil, Gökhan S. "Inflammation, metaflammation and immunometabolic disorders." Nature 542, no. 7640 (February 2017): 177–85. http://dx.doi.org/10.1038/nature21363.

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Furuhashi, Masato, Shutaro Ishimura, Hideki Ota, and Tetsuji Miura. "Lipid Chaperones and Metabolic Inflammation." International Journal of Inflammation 2011 (2011): 1–12. http://dx.doi.org/10.4061/2011/642612.

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Анотація:

Over the past decade, a large body of evidence has emerged demonstrating an integration of metabolic and immune response pathways. It is now clear that obesity and associated disorders such as insulin resistance and type 2 diabetes are associated with a metabolically driven, low-grade, chronic inflammatory state, referred to as “metaflammation.” Several inflammatory cytokines as well as lipids and metabolic stress pathways can activate metaflammation, which targets metabolically critical organs and tissues including adipocytes and macrophages to adversely affect systemic homeostasis. On the other hand, inside the cell, fatty acid-binding proteins (FABPs), a family of lipid chaperones, as well as endoplasmic reticulum (ER) stress, and reactive oxygen species derived from mitochondria play significant roles in promotion of metabolically triggered inflammation. Here, we discuss the molecular and cellular basis of the roles of FABPs, especially FABP4 and FABP5, in metaflammation and related diseases including obesity, diabetes, and atherosclerosis.

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Muskiet, Frits A. J., Pedro Carrera-Bastos, Leo Pruimboom, Alejandro Lucia, and David Furman. "Obesity and Leptin Resistance in the Regulation of the Type I Interferon Early Response and the Increased Risk for Severe COVID-19." Nutrients 14, no. 7 (March 26, 2022): 1388. http://dx.doi.org/10.3390/nu14071388.

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Obesity, and obesity-associated conditions such as hypertension, chronic kidney disease, type 2 diabetes, and cardiovascular disease, are important risk factors for severe Coronavirus disease-2019 (COVID-19). The common denominator is metaflammation, a portmanteau of metabolism and inflammation, which is characterized by chronically elevated levels of leptin and pro-inflammatory cytokines. These induce the “Suppressor Of Cytokine Signaling 1 and 3” (SOCS1/3), which deactivates the leptin receptor and also other SOCS1/3 sensitive cytokine receptors in immune cells, impairing the type I and III interferon early responses. By also upregulating SOCS1/3, Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2 adds a significant boost to this. The ensuing consequence is a delayed but over-reactive immune response, characterized by high-grade inflammation (e.g., cytokine storm), endothelial damage, and hypercoagulation, thus leading to severe COVID-19. Superimposing an acute disturbance, such as a SARS-CoV-2 infection, on metaflammation severely tests resilience. In the long run, metaflammation causes the “typical western” conditions associated with metabolic syndrome. Severe COVID-19 and other serious infectious diseases can be added to the list of its short-term consequences. Therefore, preventive measures should include not only vaccination and the well-established actions intended to avoid infection, but also dietary and lifestyle interventions aimed at improving body composition and preventing or reversing metaflammation.

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Egger, Garry, and John Dixon. "Obesity and chronic disease: always offender or often just accomplice?" British Journal of Nutrition 102, no. 8 (May 18, 2009): 1238–42. http://dx.doi.org/10.1017/s0007114509371676.

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Over a decade ago, the finding of a form of low-grade systemic inflammation (‘metaflammation’) associated with obesity, insulin resistance and chronic disease proffered a causal explanation for the latter. However, recent work has shown that metaflammation is also associated with several modern lifestyle-related and environmental inducers, with or without obesity. Here, we present accumulating data to show a link between metaflammation and a number of non-microbial environmental and lifestyle stimulants, both with and without obesity. This implies that obesity may often be an accomplice to, as much as an offender in, major metabolic disease. The real (albeit distal) cause of such a disease appears to lie in aspects of the modern techno-industrial environment driving unhealthy lifestyle behaviours. If true, this suggests that while individual weight loss may be a component of chronic disease management, it may be neither ‘necessary’ nor ‘sufficient’ to reduce the problem at a population level. Greater multidisciplinary and policy input is needed to modify the economic and political drivers of the modern, obesogenic environment.

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Tufanli, Ozlem, Pelin Telkoparan Akillilar, Diego Acosta-Alvear, Begum Kocaturk, Umut Inci Onat, Syed Muhammad Hamid, Ismail Çimen, Peter Walter, Christian Weber, and Ebru Erbay. "Targeting IRE1 with small molecules counteracts progression of atherosclerosis." Proceedings of the National Academy of Sciences 114, no. 8 (January 30, 2017): E1395—E1404. http://dx.doi.org/10.1073/pnas.1621188114.

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Metaflammation, an atypical, metabolically induced, chronic low-grade inflammation, plays an important role in the development of obesity, diabetes, and atherosclerosis. An important primer for metaflammation is the persistent metabolic overloading of the endoplasmic reticulum (ER), leading to its functional impairment. Activation of the unfolded protein response (UPR), a homeostatic regulatory network that responds to ER stress, is a hallmark of all stages of atherosclerotic plaque formation. The most conserved ER-resident UPR regulator, the kinase/endoribonuclease inositol-requiring enzyme 1 (IRE1), is activated in lipid-laden macrophages that infiltrate the atherosclerotic lesions. Using RNA sequencing in macrophages, we discovered that IRE1 regulates the expression of many proatherogenic genes, including several important cytokines and chemokines. We show that IRE1 inhibitors uncouple lipid-induced ER stress from inflammasome activation in both mouse and human macrophages. In vivo, these IRE1 inhibitors led to a significant decrease in hyperlipidemia-induced IL-1β and IL-18 production, lowered T-helper type-1 immune responses, and reduced atherosclerotic plaque size without altering the plasma lipid profiles in apolipoprotein E-deficient mice. These results show that pharmacologic modulation of IRE1 counteracts metaflammation and alleviates atherosclerosis.

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Napitupulu, Rosalia E., Anna Meiliana, and Andi Wijaya. "Correlation of Progranulin, Granulin, Adiponectin and Vaspin with Metaflammation (hs-CRP) in Indonesian Obese Men." Indonesian Biomedical Journal 5, no. 2 (August 1, 2013): 107. http://dx.doi.org/10.18585/inabj.v5i2.59.

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BACKGROUND: Obesity is closely related to chronic, low grade systemic inflammation (metaflammation) and it leads to further metabolic complications such as hypertension, atherosclerosis, and type 2 diabetes due to the adipocytokine imbalance. This study was carried out to assess the correlation between progranulin, granulin, adiponectin and visceral adipose tissue-derived serine protease inhibitor (Vaspin) with metaflammation (high sensitivity C-reactive protein (hs-CRP)) in centrally obese men.METHODS: This study was observational with a cross sectional design involving 60 men aged 30-60 years, consisted of 43 obese men (waist circumference (WC) ≥90 cm) and 13 non obese men (WC <90 cm), with no hypertension, and no renal dysfunction. Anthropometric parameters, creatinine, serum glutamic oxaloacetic transferase (SGOT), serum glutamic piruvic transferase (SGPT) and hs-CRP levels were measured. Serum concentrations of progranulin, granulin, adiponectin and Vaspin were measured by ELISA.RESULTS: This study showed in obese men a significant correlation between hs-CRP and Vaspin (r=0.305; p=0.046), non-significant correlation between hs-CRP and progranulin (r=0.048; p=0.758), between hs-CRP and granulin (r=-0.223; p=0.150), also between hs-CRP and adiponectin (r=-0.121; p=0.439). Similar patterns were observed between adipokines level and WC. There were 3 patterns showing increase or decrease of adipokines value with WC between 80-86 cm; subsequently the pattern tended to become flat with WC between 86-105 cm, then showing increase or decrease of adipokines value with WC >105 cm.CONCLUSION: We found metaflammation (hs-CRP) was significantly correlated with Vaspin, but not with progranulin, granulin and adiponectin, in obese men. We suggest the possibility of a dynamic expression of adipokines related to WC that are subjected to adipocytes hypertrophy-hyperplasia phenomenon.KEYWORDS: progranulin, granulin, adiponectin, Vaspin, hs-CRP, metaflammation, central obesity

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Paccoud, Romain, Céline Saint-Laurent, Enzo Piccolo, Mylène Tajan, Alizée Dortignac, Ophélie Pereira, Sophie Le Gonidec, et al. "SHP2 drives inflammation-triggered insulin resistance by reshaping tissue macrophage populations." Science Translational Medicine 13, no. 591 (April 28, 2021): eabe2587. http://dx.doi.org/10.1126/scitranslmed.abe2587.

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Insulin resistance is a key event in type 2 diabetes onset and a major comorbidity of obesity. It results from a combination of fat excess–triggered defects, including lipotoxicity and metaflammation, but the causal mechanisms remain difficult to identify. Here, we report that hyperactivation of the tyrosine phosphatase SHP2 found in Noonan syndrome (NS) led to an unsuspected insulin resistance profile uncoupled from altered lipid management (for example, obesity or ectopic lipid deposits) in both patients and mice. Functional exploration of an NS mouse model revealed this insulin resistance phenotype correlated with constitutive inflammation of tissues involved in the regulation of glucose metabolism. Bone marrow transplantation and macrophage depletion improved glucose homeostasis and decreased metaflammation in the mice, highlighting a key role of macrophages. In-depth analysis of bone marrow–derived macrophages in vitro and liver macrophages showed that hyperactive SHP2 promoted a proinflammatory phenotype, modified resident macrophage homeostasis, and triggered monocyte infiltration. Consistent with a role of SHP2 in promoting inflammation-driven insulin resistance, pharmaceutical SHP2 inhibition in obese diabetic mice improved insulin sensitivity even better than conventional antidiabetic molecules by specifically reducing metaflammation and alleviating macrophage activation. Together, these results reveal that SHP2 hyperactivation leads to inflammation-triggered metabolic impairments and highlight the therapeutical potential of SHP2 inhibition to ameliorate insulin resistance.

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Kanbay, Mehmet, Aslihan Yerlikaya, Alan A. Sag, Alberto Ortiz, Masanari Kuwabara, Adrian Covic, Andrzej Wiecek, Peter Stenvinkel, and Baris Afsar. "A journey from microenvironment to macroenvironment: the role of metaflammation and epigenetic changes in cardiorenal disease." Clinical Kidney Journal 12, no. 6 (September 18, 2019): 861–70. http://dx.doi.org/10.1093/ckj/sfz106.

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Abstract Chronic non-communicable diseases have become a pandemic public problem in the 21st century, causing enormous burden on the economy, health and quality of life of societies. The role of a chronic inflammatory state in the pathogenesis of chronic disease has been more comprehensively recognized by recent findings. The new paradigm ‘metaflammation’ focuses on metabolism-induced (high fat or fructose-based diet or excessive calorie intake) chronic inflammation. There is a close correlation between the increased incidence of chronic kidney disease (CKD) and chronic heart failure with both increased inflammatory marker levels and western-type diet. In this review we describe the concept of metaflammation, its role in the development of CKD and chronic heart disease, the molecular and signalling pathways involved and the therapeutic consequences.

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Більше джерел

Дисертації з теми "Metaflammation"

Delépine, Chloé. "L’Interleukine 34 produite dans le pancréas, régule l’inflammation locale." Electronic Thesis or Diss., Angers, 2023. https://dune.univ-angers.fr/documents/dune17687.

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L’interleukine 34 est une cytokine décrite comme un second ligand pour le récepteur au M-CSF, CD115. Elle a été identifiée comme majoritairement produite au niveau de la peau et du cerveau où elle participe à la maintenance des cellules de Langerhans et de la microglie, respectivement. L’IL-34 est identifiée comme surexprimée dans de nombreuses pathologies inflammatoires. Dans notre étude, nous avons observé une expression constitutive de l’IL-34 dans les îlots de Langerhans humains et murins. L’analyse des effets de l’invalidation du gène de l’Il34 dans les cellules β dans un modèle de souris mise en place au laboratoire (IL-34Δpdx) a mis en évidence un rôle de la cytokine dans l’immunité locale. En vieillissant, les souris IL-34Δpdx présentent une altération de la tolérance au glucose associée à une inflammation locale plus prononcée que les souris contrôles. Ce phénotype est exacerbé quand les souris sont soumises à un régime riche en graisse et en sucre. La sécrétion d’insuline par les îlots de Langerhans des souris contrôles est altérée en présence de cytokines pro-inflammatoire. L’ajout d’IL-34 restaure la sécrétion d’insuline. En outre, la production d’IL-34 est augmentée chez les patients diabétiques de type 2. Ces résultats suggèrent que l’IL-34 synthétisée localement dans les îlots de Langerhans aurait un rôle protecteur dans un contexte inflammatoire chronique
Interleukin 34 (IL-34) is a cytokine described as a second ligand for the M-CSF receptor, CD115. IL-34 has been identified as predominantly produced in the skin and brain, where it is involved in the maintenance of Langerhans cells and microglia. IL-34 has been identified as overexpressed in several inflammatory pathologies. In our study, we observed a constitutive expression of IL-34 in human and murine Langerhans islets. Analysis of Il34 gene invalidation effects in β cells in a mouse model (IL-34Δpdx) highlighted a role for the cytokine in local immunity.As they aged, IL-34Δpdx mice showed impaired glucose tolerance associated with more pronounced local inflammation than control mice. This phenotype is exacerbated when mice are subjected to a high-fat diet. Insulin secretion from the islets of control mice is impaired in the presence of pro-inflammatory cytokines. The addition of IL-34 restores insulin release. Moreover, IL-34 production is increased in type 2 diabetic patients.These results support the idea of a protective role for IL-34 locally in pancreatic islets in a chronic inflammatory context

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Частини книг з теми "Metaflammation"

"9 Metaflammation: eine Entzündung ausgelöst durch Nährstoffspeicherungen." In Orale Präventivmedizin, edited by René B. A. Sanderink, Heinz H. Renggli, and Ulrich P. Saxer. Stuttgart: Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/b-0042-184319.

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Тези доповідей конференцій з теми "Metaflammation"

Yoshimura, Tania M., Ilka T. Kato, Alessandro M. Deana, and Martha S. Ribeiro. "Treating metabolic syndrome’s metaflammation with low level light therapy: preliminary results." In SPIE BiOS, edited by Michael R. Hamblin, James D. Carroll, and Praveen Arany. SPIE, 2014. http://dx.doi.org/10.1117/12.2040901.

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Ghadimi, D., A. Nielsen, M. Farghaly Yoness Hassan, R. Fölster-Holst, M. de Vrese та KJ Heller. "Modulation of GSK – 3β/β – catenin cascade by commensal bifidobateria plays an important role for the inhibition of metaflammation-related biomarkers in response to LPS or non-physiological concentrations of fructose: An in vitro study". У 47. Jahrestagung der Gesellschaft für Gastroenterologie in Bayern e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688867.

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