心脏毒性
阿霉素
医学
不利影响
心肌病
癌症研究
心力衰竭
内皮功能障碍
内科学
心脏病学
化疗
作者
Melissa Cobb,Shixin Tao,Katherine Shortt,Magdy Girgis,Jeryl Hauptman,Jill Schriewer,Zaphrirah Chin,Edward Dorfman,Kyle Campbell,Daniel P. Heruth,Ralph V. Shohet,Buddhadeb Dawn,Eugene Konorev
出处
期刊:American Journal of Physiology-heart and Circulatory Physiology
[American Physiological Society]
日期:2022-12-01
卷期号:323 (6): H1091-H1107
被引量:3
标识
DOI:10.1152/ajpheart.00312.2022
摘要
Microvascular endothelial cells in the heart accumulate more intravenously administered doxorubicin than nonendothelial cardiac cell types. The treatment enhanced the TGF-β/Smad3 pathway and elicited endothelial cell senescence and inflammatory responses followed by adverse cardiac remodeling and dysfunction in wild-type but not Smad3-deficient animals. Our study suggests that the TGF-β/Smad3 pathway contributes to the development of doxorubicin cardiomyopathy and the potential value of novel approaches to ameliorate cardiotoxicity by targeting the Smad3 transcription factor.
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