通过AMFR激活ER-phagy可以通过mTORC1通路减轻心脏纤维化和心肌梗塞后心肌梗塞

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Updated: Sep 15, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

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Zhixiang Wang1, Kaifan Niu1,2, Wei Liu1

  • 1Department of Cardiology, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)
|July 17, 2025
PubMed
概括

自克林运动因子受体 (AMFR) 通过增强ER-phagy来抑制心肌梗塞后的心肌纤维化. AMFR调节FAM134B的循环,减少纤维细胞激活,改善心脏功能.

关键词:
美国空军飞行飞行器 (AMFR)这就是ER-phagy.在FAM134B中.纤维细胞激活的激活在 mTORC1 的情况下,mTORC1 是心肌梗塞的心脏病发作

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