| First Author | Zheng WF | Year | 2019 |
| Journal | J Cell Biochem | Volume | 120 |
| Issue | 6 | Pages | 10748-10755 |
| PubMed ID | 30719766 | Mgi Jnum | J:295831 |
| Mgi Id | MGI:6454565 | Doi | 10.1002/jcb.28366 |
| Citation | Zheng WF, et al. (2019) C1qTNF-related protein-6 protects against doxorubicin-induced cardiac injury. J Cell Biochem 120(6):10748-10755 |
| abstractText | 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. |
