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C1qTNF‐related protein‐6 protects against doxorubicin‐induced cardiac injury
Author(s) -
Zheng WeiFeng,
Zhang ShouYan,
Ma HuiFang,
Chang XueWei,
Wang Hao
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28366
Subject(s) - cardiotoxicity , doxorubicin , protein kinase b , apoptosis , cardiac function curve , pharmacology , downregulation and upregulation , in vivo , heart failure , medicine , biology , toxicity , biochemistry , chemotherapy , microbiology and biotechnology , gene
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.