Omentin protects H9c2 cells against docetaxel cardiotoxicity

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-relat...

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Detalhes bibliográficos
Autores: Lage Fernández, Ricardo, Cebro Márquez, María, Rodríguez Mañero, Moises, González Juanatey, José Ramón, Moscoso Galán, Isabel
Tipo de documento: artigo
Data de publicação:2019
País:España
Recursos:Servizo Galego de Saúde (SERGAS)
Repositório:RUNA. Repositorio da Consellería de Sanidade e Sergas
OAI Identifier:oai:runa.sergas.gal:20.500.11940/15487
Acesso em linha:https://www.ncbi.nlm.nih.gov/pubmed/30794687
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386316/pdf/pone.0212782.pdf
http://hdl.handle.net/20.500.11940/15487
Access Level:Acceso aberto
Palavra-chave:CHUS
IDIS
Descrição
Resumo: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.