C1qTNF-related protein-6 protects against doxorubicin-induced cardiac injury.
J Cell Biochem
; 120(6): 10748-10755, 2019 06.
Article
em En
| MEDLINE
| ID: mdl-30719766
ABSTRACT
The clinical use of doxorubicin (DOX) is limited by its toxic effect. However, there is no specific drug that can prevent DOX-related cardiac injury. C1qTNF-related protein-6 (CTRP6) is a newly identified adiponectin paralog with many protective functions on metabolism and cardiovascular diseases. However, little is known about the effect of CTRP6 on DOX-induced cardiac injury. The present study aimed to investigate whether CTRP6 could protect against DOX-related cardiotoxicity. To induce acute cardiotoxicity, the mice were intraperitoneally injected with a single dose of DOX (15 mg/kg). Cardiomyocyte-specific CTRP6 overexpression was achieved using an adenoassociated virus system at 4 weeks before DOX injection. The data in our study demonstrated that CTRP6 messenger RNA and protein expression were decreased in DOX-treated hearts. CTRP6 attenuated cardiac atrophy induced by DOX injection and inhibited cardiac apoptosis and improved cardiac function in vivo. CTRP6 also promoted the activation of protein kinase B (AKT/PKB) signaling pathway in DOX-treated mice. CTRP6 prevented cardiomyocytes from DOX-induced apoptosis and activated the AKT pathway in vitro. CTRP6 lost its protection against DOX-induced cardiac injury in mice with AKT inhibition. In conclusion, CTRP6 protected the heart from DOX-cardiotoxicity and improves cardiac function via activation of the AKT signaling pathway.
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Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Doxorrubicina
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Miócitos Cardíacos
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Proteínas Proto-Oncogênicas c-akt
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Adipocinas
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Cardiotoxicidade
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Traumatismos Cardíacos
Tipo de estudo:
Etiology_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article