期刊
JACC-BASIC TO TRANSLATIONAL SCIENCE
卷 8, 期 8, 页码 992-1007出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacbts.2023.02.014
关键词
apoptosis; cardiomyopathy; doxorubicin; interferon-gamma; natural killer T cells
This study found that activation of iNKT cells attenuated Doxorubicin-induced cardiomyocyte death and cardiac dysfunction. This effect may be mediated through increased interferon-γ and phosphorylation of signal transducers and activators of transcription 1 and extracellular signal-regulated kinase.
Doxorubicin (DOX)-induced cardiomyopathy has poor prognosis, and myocardial inflammation is intimately involved in its pathophysiology. The role of invariant natural killer T (iNKT) cells has not been fully determined in this disease. We here demonstrated that activation of iNKT cells by a-galactosylceramide (GC) attenuated DOXinduced cardiomyocyte death and cardiac dysfunction. aGC increased interferon (IFN)-g and phosphorylation of signal transducers and activators of transcription 1 (STAT1) and extracellular signal-regulated kinase (ERK). Administration of anti-IFN-g neutralizing antibody abrogated the beneficial effects of aGC on DOX-induced cardiac dysfunction. These findings emphasize the protective role of iNKT cells in DOX-induced cardiomyopathy via the IFN-g-STAT1-ERK pathway. (J Am Coll Cardiol Basic Trans Science 2023;8:992-1007)& COPY; 2023 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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