MAPK/ERK通路
STAT1
信号转导
干扰素
激酶
炎症
癌症研究
心肌病
免疫学
阿霉素
医学
化学
生物
细胞生物学
心力衰竭
化疗
内科学
作者
Masafumi Sada,Shouji Matsushima,Masataka Ikeda,Soichiro Ikeda,Kazuto Okabe,Ayako Ishikita,Tomonori Tadokoro,Nobuyuki Enzan,Taishi Yamamoto,Hiroko Deguchi Miyamoto,Yoshitomo Tsutsui,Ryo Miyake,Daiki Setoyama,Dongchon Kang,Tomomi Ide,Hiroyuki Tsutsui
标识
DOI:10.1016/j.jacbts.2023.02.014
摘要
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 α-galactosylceramide (GC) attenuated DOX-induced cardiomyocyte death and cardiac dysfunction. αGC increased interferon (IFN)-γ and phosphorylation of signal transducers and activators of transcription 1 (STAT1) and extracellular signal-regulated kinase (ERK). Administration of anti-IFN-γ neutralizing antibody abrogated the beneficial effects of αGC on DOX-induced cardiac dysfunction. These findings emphasize the protective role of iNKT cells in DOX-induced cardiomyopathy via the IFN-γ-STAT1-ERK pathway.
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