Theranostics 2018; 8(4):874-877. doi:10.7150/thno.23364 This issue


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

Matthias S. Leisegang1,2✉

1. Goethe-University, Institute for Cardiovascular Physiology, Frankfurt am Main, Germany;
2. German Center of Cardiovascular Research (DZHK), Partner site RheinMain, Frankfurt, Germany

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Leisegang MS. LET's sponge: How the lncRNA PFL promotes cardiac fibrosis. Theranostics 2018; 8(4):874-877. doi:10.7150/thno.23364. Available from

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Graphic abstract

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.

Keywords: LncRNA, PFL, miRNA, ceRNA, Cardiac Fibrosis