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Relevant bibliographies by topics / Metaflammation

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Journal articles

Academic literature on the topic 'Metaflammation'

Author: Grafiati

Published: 13 April 2024

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Journal articles on the topic "Metaflammation"

1

Wei, Lisha, Yan-Yan Zheng, Jie Sun, et al. "GGPP depletion initiates metaflammation through disequilibrating CYB5R3-dependent eicosanoid metabolism." Journal of Biological Chemistry 295, no. 47 (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 wit

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2

Embgenbroich, Maria, Hendrik J. P. van der Zande, Leonie Hussaarts, et al. "Soluble mannose receptor induces proinflammatory macrophage activation and metaflammation." Proceedings of the National Academy of Sciences 118, no. 31 (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 weigh

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3

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

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4

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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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 ot

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5

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 (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

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6

Egger, Garry, and John Dixon. "Obesity and chronic disease: always offender or often just accomplice?" British Journal of Nutrition 102, no. 8 (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

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7

Tufanli, Ozlem, Pelin Telkoparan Akillilar, Diego Acosta-Alvear, et al. "Targeting IRE1 with small molecules counteracts progression of atherosclerosis." Proceedings of the National Academy of Sciences 114, no. 8 (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

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8

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 (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 year

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9

Paccoud, Romain, Céline Saint-Laurent, Enzo Piccolo, et al. "SHP2 drives inflammation-triggered insulin resistance by reshaping tissue macrophage populations." Science Translational Medicine 13, no. 591 (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 p

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10

Kanbay, Mehmet, Aslihan Yerlikaya, Alan A. Sag, et al. "A journey from microenvironment to macroenvironment: the role of metaflammation and epigenetic changes in cardiorenal disease." Clinical Kidney Journal 12, no. 6 (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

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