IL-27p28 knockout aggravates Doxorubicin-induced cardiotoxicity by regulating Macrophage polarization

Feng, Yanqin; Ji, Qingwei; Ye, Di; Pan, Heng; Lu, Xiyi; Liren, Gan; Wang, Menglong; Liu, Jianfang; Xu, Yao; Zhang, Jishou; Zhao, Mengmeng; Xu, Shou-Xi; Yin, Zheng; Pan, Wei; Wei, Cheng; Liu, Meilin; Wan, Jun; Ye, Jing

doi:10.1016/j.bcp.2023.115469

Biochemical Pharmacology

2023

DOI: 10.1016/j.bcp.2023.115469

|View full text |Cite

IL-27p28 knockout aggravates Doxorubicin-induced cardiotoxicity by regulating Macrophage polarization

Yanqin Feng

Qingwei Ji

Di Ye

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2024

Publication Types

Select...

Article1

Relationship

Self Cite0

Independent1

Authors

Journals

Cited by 1 publication

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Possible pathogenic mechanisms for doxorubicin‐induced splenic atrophy in a human breast cancer xenograft mouse model

Xue,

Ye,

Sun

2024

J of Applied Toxicology

View full text Add to dashboard Cite

Doxorubicin‐based chemotherapy is a widely used first‐line treatment for breast cancer, yet it is associated with various side effects, including splenic atrophy. However, the pathogenic mechanisms underlying doxorubicin‐induced atrophy of the spleen remain unclear. This study investigates that doxorubicin treatment leads to splenic atrophy through several interconnected pathways involving histological changes, an inflammatory response, and apoptosis. Immunohistochemical and western blot analyses revealed reduced size of white and red pulp, decreased cellularity, amyloidosis, and fibrotic remodeling in the spleen following doxorubicin treatment. Additionally, increased secretion of pro‐inflammatory cytokines was detected using an antibody array and enzyme‐linked immunosorbent assay (ELISA), which triggers inflammation through the regulation of signal transducer and activator of transcription 3 (STAT3) and nuclear factor‐kappa B (NF‐κB) signaling pathways. Further analysis revealed that the loss of regulators and effectors of the oxidative defense system, including sirtuin (Sirt)3, Sirt5, superoxide dismutase (SOD)1, and SOD2, was implicated in the upstream regulation of caspase‐dependent cellular apoptosis. These findings provide insights on the pathogenic mechanisms underlying doxorubicin‐induced splenic atrophy and suggest that further investigation may be warranted to explore strategies for managing potential side effects in breast cancer patients treated with doxorubicin.

show abstract

Possible pathogenic mechanisms for doxorubicin‐induced splenic atrophy in a human breast cancer xenograft mouse model

Xue,

Ye,

Sun

2024

J of Applied Toxicology

View full text Add to dashboard Cite

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

IL-27p28 knockout aggravates Doxorubicin-induced cardiotoxicity by regulating Macrophage polarization

Cited by 1 publication

References 35 publications

Possible pathogenic mechanisms for doxorubicin‐induced splenic atrophy in a human breast cancer xenograft mouse model

Possible pathogenic mechanisms for doxorubicin‐induced splenic atrophy in a human breast cancer xenograft mouse model

Contact Info

Product

Resources

About