Macrophage-Derived Exosomal Mir-155 Regulating Cardiomyocyte Pyroptosis and Hypertrophy in Uremic Cardiomyopathy

Macrophage-Derived Exosomal Mir-155 Regulating Cardiomyocyte Pyroptosis and Hypertrophy in Uremic Cardiomyopathy
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巨噬细胞衍生的外泌体 Mir-155 调节尿毒症心肌病心肌细胞焦亡和肥大

DOI:
10.1016/j.jacbts.2019.10.011
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发表时间:
2020-01
期刊:
JACC: Basic to Translational Science
影响因子:
--
通讯作者:
Bi-Cheng Liu
Bi-Cheng Liu
中科院分区:
其他
文献类型:
--
作者:
Bin Wang;Ze-Mu Wang;Jia-Ling Ji;Weihua Gan;Aiqing Zhang;Hao-Jie Shi;Hao Wang;Linli Lv;Zuolin Li;Taotao Tang;Jie Du;Xiaonan H. Wang;Bi-Cheng Liu

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合成miR-155并将其加载到外泌体中,以增加尿毒症心脏中巨噬细胞的浸润。释放的外泌体与质膜融合导致miR-155释放到胞质溶胶中,并导致心肌细胞中O类叉头转录因子(FoxO 3a)的翻译抑制。最后,巨噬细胞衍生的含miR-155的外泌体通过直接靶向尿毒症小鼠中的FoxO 3a促进心肌细胞焦亡和尿毒症心肌病变化(心脏肥大和纤维化)。
miR-155 was synthesized and loaded into exosomes in increased infiltration of macrophages in a uremic heart. The released exosomal fusion with the plasma membrane leads to the release of miR-155 into the cytosol and translational repression of forkhead transcription factors of the O class (FoxO3a) in cardiomyocytes. Finally, macrophage-derived miR-155–containing exosomes promoted cardiomyocyte pyroptosis and uremic cardiomyopathy changes (cardiac hypertrophy and fibrosis) by directly targeting FoxO3a in uremic mice.
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