Lnc-Ang362 is a pro-fibrotic long non-coding RNA promoting cardiac fibrosis after myocardial infarction by suppressing Smad7

Lnc-Ang362 is a pro-fibrotic long non-coding RNA promoting cardiac fibrosis after myocardial infarction by suppressing Smad7

Cardiac fibrosis following myocardial infarction (MI) leads to cardiac remodeling and dysfunction. Dysregulation of Smad7 which negatively regulates the profibrotic transforming growth factor-β1 (TGF-β1)/Smad signaling promotes cardiac fibrosis. However, the molecular mechanisms underlying TGF-β1/Sm...

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Veröffentlicht in:Archives of biochemistry and biophysics 2020-05, Vol.685, p.108354-108354, Article 108354
Hauptverfasser: Chen, Guo, Huang, Sihui, Song, Feier, Zhou, Yingling, He, Xuyu
Format: Artikel
Sprache:eng
Schlagworte:
Cardiac fibrosis
Long non-coding RNA
Myocardial infarction
Smad7
Transforming growth factor-β1
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Zusammenfassung:Cardiac fibrosis following myocardial infarction (MI) leads to cardiac remodeling and dysfunction. Dysregulation of Smad7 which negatively regulates the profibrotic transforming growth factor-β1 (TGF-β1)/Smad signaling promotes cardiac fibrosis. However, the molecular mechanisms underlying TGF-β1/Smad7 dysregulation remain elusive. Long non-coding RNAs (lncRNAs) are recently emerging as important regulators of cardiac diseases. Here, we report lnc-Ang362 is a novel lncRNA mediating MI-induced fibrosis through TGF-β1/Smad7 signaling pathway. The MI model was established by artificial coronary artery occlusion in rats. Microarray analysis identified 215 lncRNAs (fold change > 2.0, P 
ISSN:0003-9861
1096-0384
DOI:10.1016/j.abb.2020.108354