ArticleInternational journal of clinical and experimental pathology2020
Long non-coding RNA BANCR promotes interferon-β-induced cardiomyocyte apoptosis by targeting signal transducer and activator of transcription 1
Article in International journal of clinical and experimental pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Interaction Between Non-Coding RNAs and Interferons: With an Especial Focus on Type I Interferons.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardium functions as an immune organ, and myocardial ischemia-reperfusion (I/R) is known to initiate myocardial innate immune response to induce myocardial injury. However, the mechanisms underlying interferon-β (IFN-β)-mediated myocardial injury during I/R and whether long non-coding RNAs (lncRNAs) are involved in IFN-β-mediated myocardial injury remain unknown. This study identified that I/R significantly induced IFN-β expression in induced pluripotent stem cell-derived cardiomyocytes, and IFN-β further enhanced I/R-induced myocardial apoptosis. Furthermore, it was demonstrated that the lncRNA BRAF-activated non-coding RNA (BANCR) was highly expressed in cardiomyocytes, and BANCR-knockdown suppressed signal transducer and activator of transcription 1 (STAT1) phosphorylation and IFN-β-induced cardiomyocyte apoptosis. Furthermore, it was identified that BANCR specifically interacted with STAT1 to promote IFN-β-STAT1 signaling and enhanced the expression of pro-apoptotic interferon stimulated genes. Overall, the present study reports that lncRNA BANCR promotes IFN-β-mediated cardiomyocyte apoptosis following I/R injury by interacting with STAT1, suggesting lncRNA BANCR is involved in IFN-β-induced cardiomyocyte apoptosis.
Indexed as
Identifiers
33284897PMC7716135W3111405420What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.