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Updated: Sep 9, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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CPNE5の過剰発現は,FAS受容体の分解を促進することによって,心筋細胞のアポトーシスを阻害する

Tingting Zhao1, Yangjinming Bai1, Yudong Fei1

  • 1Department of Cardiology, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, China.

iScience
|September 2, 2025
PubMed
まとめ

コピン5 (CPNE5) の過剰発現は,細胞死と線維症を減少させることで,心臓を損傷から保護する. これは,ER-ファージ経路経由でFASの分解を促進し,ストレス中に心筋細胞を保護することによって達成されます.

キーワード:
生物科学ネズミの心臓病ネズミの分子生物学

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