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Update on the pathophysiological activities of the cardiac molecule cardiotrophin-1 in obesity

Dallegri, Franco
Published in Mediators of Inflammation. 2013, vol. 2013, p. 370715
Abstract Cardiotrophin-1 (CT-1) is a heart-targeting cytokine that has been reported to exert a variety of activities also in other organs such as the liver, adipose tissue, and atherosclerotic arteries. CT-1 has been shown to induce these effects via binding to a transmembrane receptor, comprising the leukaemia inhibitory factor receptor (LIFR β ) subunit and the glycoprotein 130 (gp130, a common signal transducer). Both local and systemic concentrations of CT-1 have been shown to potentially play a critical role in obesity. For instance, CT-1 plasma concentrations have been shown to be increased in metabolic syndrome (a cluster disease including obesity) probably due to adipose tissue overexpression. Interestingly, treatment with exogenous CT-1 has been shown to improve lipid and glucose metabolism in animal models of obesity. These benefits might suggest a potential therapeutic role for CT-1. However, beyond its beneficial properties, CT-1 has been also shown to induce some adverse effects, such as cardiac hypertrophy and adipose tissue inflammation. Although scientific evidence is still needed, CT-1 might be considered as a potential example of damage/danger-associated molecular pattern (DAMP) in obesity-related cardiovascular diseases. In this narrative review, we aimed at discussing and updating evidence from basic research on the pathophysiological and potential therapeutic roles of CT-1 in obesity.
Keywords Adipose Tissue/drug effects/immunology/metabolismAnimalsCytokines/metabolism/pharmacologyHumansLipid Metabolism/drug effectsMetabolic Syndrome X/metabolismObesity/metabolismSignal Transduction/physiology
PMID: 23690661
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Research groups Ophtalmologie expérimentale (925)
L'athérosclérose et ses complications cliniques (591)
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ASRIH, Mohamed et al. Update on the pathophysiological activities of the cardiac molecule cardiotrophin-1 in obesity. In: Mediators of Inflammation, 2013, vol. 2013, p. 370715. doi: 10.1155/2013/370715 https://archive-ouverte.unige.ch/unige:77516

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Deposited on : 2015-11-23

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