Omentin protects H9c2 cells against docetaxel cardiotoxicity
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PLOS
Abstract
Background : Association between obesity and cardiovascular diseases is well known, however increased susceptibility of obese patients to develop several cancer types is not so commonly known. Current data suggest that poorer overall survival in cancer patients might be associated to non-cancer-related causes such as higher risk of cardiotoxicity in obese patients treated with chemotherapeutic agents. Omentin, a novel adipokine decreased in obesity, is actually in the spotlight due to its favourable effects on inflammation, glucose homeostasis and cardiovascular diseases. Also, recent data showed that in vitro anthracycline-induced cardiomyocyte apoptosis is counteracted by omentin suggesting its cardioprotective role.
Objective: Our aim was to evaluate omentin effects against docetaxel toxicity.
Results: Our data indicate that omentin inhibits docetaxel-induced viability loss and that increased viability is associated to decreased caspase-3 expression and cell death. Although omentin reduces NOX4 expression, it failed to reduce docetaxel-induced reactive oxygen species production. Our results indicate that omentin decreases docetaxel-induced endoplasmic reticulum stress, suggesting that cardioprotective role might be associated to ERS inhibition.
Conclusion : These data suggest that omentin treatment may contribute to decrease susceptibility to DTX-induced cardiotoxicity.
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Lage, R., Cebro-Márquez, M., Rodríguez-Mañero, M., González-Juanatey, J. R., & Moscoso, I. (2019). Omentin protects H9c2 cells against docetaxel cardiotoxicity. PloS One, 14(2), e0212782. doi:10.1371/journal.pone.0212782
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https://doi.org/10.1371/journal.pone.0212782Sponsors
This work was supported by Fundación Mutua Madrileña 2014 (R.L.), Red de Investigación Cardiovascular (RIC) (RD12/0042/0039) an initiative of ISCIII (J.R.G-J), Programa de Consolidación de Unidades de Investigación Competitivas do SUG (GPC 2013-051) of Xunta de Galicia (J.R.G-J) and Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV) (CB16/11/00226) of Instituto de Salud Carlos III (J.R.G-J). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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© 2019 Lage et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.








