The role of resistin as a regulator of inflammation: Implications for various human pathologies

Filková, Mária; Haluzı́k, Martin; Šenolt, Ladislav

doi:10.1016/j.clim.2009.07.013

Cited by 375 publications

(355 citation statements)

References 139 publications

(192 reference statements)

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“…In general, serum levels of adipokines are higher in RA patients compared to control (non-RA) subjects and are associated with inflammatory state of the disease [2][3][4]. There is evidence that adiponectin (in contrast to metabolic disorders) and some other adipokines, particularly visfatin and resistin, have a proinflammatory and joint-destructive role in RA by inducing proinflammatory cytokines, chemokines, and matrix degrading enzymes in synovial fibroblasts, lymphocytes, chondrocytes, and endothelial cells [12].…”

Section: Adipokines As Biomarkers Linking Obesity and Rheumatoid Arthmentioning

confidence: 99%

“…However, under pathological conditions, resident tissue cells and predominantly immune cells can contribute to local as well as systemic upregulation of adipokines [2]. Initially, adipokines were thought to be involved in energy homeostasis and metabolism, however, for well over a decade, adipokines have been shown to be implicated in chronic inflammation, cancer, and other various conditions [2]. Several adipokines have been demonstrated to modulate immune response and extracellular matrix damage.…”

Section: Introductionmentioning

confidence: 99%

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Adipokines: role in local and systemic inflammation of rheumatic diseases

Šenolt

2016

Expert Review of Clinical Immunology

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Section: Adipokines As Biomarkers Linking Obesity and Rheumatoid Arthmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Adipokines: role in local and systemic inflammation of rheumatic diseases

Šenolt

2016

Expert Review of Clinical Immunology

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“…Previous studies have investigated the function of resistin in mouse obesity and diabetes models, and have implicated resistin in the pathogenesis of obesity-mediated insulin resistance and type 2 diabetes (3,12,13). Moreover, it has been reported that resistin is closely associated with inflammation (14)(15)(16). Resistin regulates the synthesis and secretion of proinflammatory cytokines such as tumor necrosis factor α (TNF-α), interleukin-6 (IL-6) and IL-1β in macrophages via a nuclear factor κB (NF-κB)-dependent pathway (17)(18)(19)(20), but the specific receptor of resistin in vivo has not yet been identified.…”

Section: Introductionmentioning

confidence: 99%

Resistin increases the expression of NOD2 in mouse monocytes

Ren

Taomei

Zuo

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Previous studies have indicated that resistin, a type of adipokine, contributes to the development of insulin resistance and type 2 diabetes mellitus, and mediates inflammatory reactions. However, a specific receptor for resistin has not yet been identified. In this study, the relationship between resistin and nucleotide-binding oligomerization domain-like receptors, as well as resistin signal transduction, was examined through transfection, quantitative polymerase chain reaction, western blot analysis and ELISA. The mRNA expression of nucleotide-binding oligomerization domain-containing protein 2 (NOD2), a key immune receptor related to insulin resistance, was significantly increased by resistin treatment at concentrations of 100, 150 and 200 ng/ml (P<0.05, P<0.01 and P<0.01, respectively). The mRNA expression of downstream signaling molecules in the NOD2 signaling pathway, receptor-interacting serine/threonine-protein kinase 2 (RIP2; P<0.01 at 6, 12 and 24 h) and inhibitor of NF-κB kinase subunit beta (P<0.01 at 3, 6, 12 and 24 h) were significantly increased by resistin treatment compared with the control. The mRNA expression of key proinflammatory cytokines, tumor necrosis factor α, IL (interleukin)-6 and IL-1β, were also significantly increased by resistin treatment compared with the control (P<0.01). NOD2 knockdown by small interfering RNA (siRNA) significantly decreased the expression of NOD2 and RIP2 (P<0.01), and there was no significant increase in the levels of cytokines, as compared with treatment with control siRNA. These findings indicate that the inflammatory reaction induced by resistin involves the NOD2-nuclear factor (NF)-κB signaling pathway. The inhibition of NF-κB significantly decreased the secretion of key inflammatory cytokines (P<0.01), suggesting that NF-κB signaling mechanisms are essential to the resistin-induced inflammatory response.

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“…El exceso o déficit del TA resultará en una producción o liberación alterada de los mediadores antes mencionados, ocasionando una comunicación defectuosa con otros órganos, alteraciones en el metabolismo y el desarrollo posterior de enfermedades endocrino-metabólicas. Un exceso de TA en la región visceral se ha asociado con insulino resistina, variables de dimensión y composición corporal -A. souki et al rev Med chile 2016; 144: 307-316 resistencia (IR), DM2, dislipidemia, hiperglicemia e hipertensión, así como estados protrombóticos y proinflamatorios [4][5][6] .…”

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“…En humanos, los macrófagos son los mayores responsables de su liberación, mientras que el tejido adiposo parece contribuir con una pequeña fracción. La resistina humana es una hormona polipeptídica, de 12,5 kDa, constituida por 108 residuos de aminoácidos que pertenecen a la familia de proteínas ricas en cisteína 6,7 . En cuanto a su conformación, la resistina se presenta en formas distintas de ensamblaje, con acciones diferentes en la regulación metabólica.…”

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