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LET's sponge: How the lncRNA PFL promotes cardiac fibrosis

Compared to their protein-coding counterparts, almost nothing is known about the role of long noncoding RNAs (lncRNAs) in cardiac fibrosis. In the current report, Liang and Pan et al. characterized the pro-fibrotic lncRNA PFL in respect to cardiac fibrosis in mice. PFL was upregulated in the hearts...

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Autor principal: Leisegang, Matthias S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5817098/
https://www.ncbi.nlm.nih.gov/pubmed/29463987
http://dx.doi.org/10.7150/thno.23364
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author Leisegang, Matthias S.
author_facet Leisegang, Matthias S.
author_sort Leisegang, Matthias S.
collection PubMed
description Compared to their protein-coding counterparts, almost nothing is known about the role of long noncoding RNAs (lncRNAs) in cardiac fibrosis. In the current report, Liang and Pan et al. characterized the pro-fibrotic lncRNA PFL in respect to cardiac fibrosis in mice. PFL was upregulated in the hearts of mice after myocardial infarction and in fibrotic cardiac fibroblasts. Moreover, PFL competitively sponged the cardio-protective miRNA let-7d in cardiac fibroblasts. Knockdown of platelet activating factor receptor (PTAFR) was shown to affect the pro-fibrotic collagen production mediated by PFL. PTAFR overexpression also led to collagen production and RNA abundance of PTAFR was also regulated by miRNA let-7d. Therefore, the PFL/PTAFR/let-7d-dependent gene regulatory mechanism proposed by the authors manifests the hypothesis of competing endogenous RNAs to cardiac fibrosis.
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spelling pubmed-58170982018-02-20 LET's sponge: How the lncRNA PFL promotes cardiac fibrosis Leisegang, Matthias S. Theranostics Editorial Compared to their protein-coding counterparts, almost nothing is known about the role of long noncoding RNAs (lncRNAs) in cardiac fibrosis. In the current report, Liang and Pan et al. characterized the pro-fibrotic lncRNA PFL in respect to cardiac fibrosis in mice. PFL was upregulated in the hearts of mice after myocardial infarction and in fibrotic cardiac fibroblasts. Moreover, PFL competitively sponged the cardio-protective miRNA let-7d in cardiac fibroblasts. Knockdown of platelet activating factor receptor (PTAFR) was shown to affect the pro-fibrotic collagen production mediated by PFL. PTAFR overexpression also led to collagen production and RNA abundance of PTAFR was also regulated by miRNA let-7d. Therefore, the PFL/PTAFR/let-7d-dependent gene regulatory mechanism proposed by the authors manifests the hypothesis of competing endogenous RNAs to cardiac fibrosis. Ivyspring International Publisher 2018-01-01 /pmc/articles/PMC5817098/ /pubmed/29463987 http://dx.doi.org/10.7150/thno.23364 Text en © Ivyspring International Publisher This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
spellingShingle Editorial
Leisegang, Matthias S.
LET's sponge: How the lncRNA PFL promotes cardiac fibrosis
title LET's sponge: How the lncRNA PFL promotes cardiac fibrosis
title_full LET's sponge: How the lncRNA PFL promotes cardiac fibrosis
title_fullStr LET's sponge: How the lncRNA PFL promotes cardiac fibrosis
title_full_unstemmed LET's sponge: How the lncRNA PFL promotes cardiac fibrosis
title_short LET's sponge: How the lncRNA PFL promotes cardiac fibrosis
title_sort let's sponge: how the lncrna pfl promotes cardiac fibrosis
topic Editorial
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5817098/
https://www.ncbi.nlm.nih.gov/pubmed/29463987
http://dx.doi.org/10.7150/thno.23364
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