ArticleJournal of cellular and molecular medicine2019
Inhibition of prostaglandin E2 receptor 4 by lnc000908 to promote the endothelial-mesenchymal transition participation in cardiac remodelling.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Decoding Long Noncoding RNAs in Cardiac Development and Congenital Heart Disease: Recent Advances and Clinical Perspectives.Circulation. Genomic and precision medicine · 2026Review
- Study on the mechanism of OSM participating in myocardial fibrosis by inhibiting TGFβ-induced EndMT of cardiac microvascular endothelial cells through SPARC/SMAD signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Targeting the E Prostanoid Receptor EP4 Mitigates Cardiac Fibrosis Induced by β-Adrenergic Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Metformin regulates the effects of IR and IGF-1R methylation on mast cell activation and airway reactivity in diabetic rats with asthma through miR-152-3p/DNMT1 axis.Cell biology and toxicology · 2023Article
- Research progress of endothelial-mesenchymal transition in diabetic kidney disease.Journal of cellular and molecular medicine · 2022Review
- The lncRNA XIST/miR-150-5p/c-Fos axis regulates sepsis-induced myocardial injury via TXNIP-modulated pyroptosis.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Inhibition of prostaglandin E2 receptor 4 by lnc000908 to promote the endothelial-mesenchymal transition participation in cardiac remodelling.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (lncRNAs) have emerged as potent regulators of cardiac disease; however, the role of lncRNA in cardiac fibrosis remains partially understood. In this study, we identified a cardiac endothelial-enriched lncRNA-lnc000908, which was markedly up-regulated in rats with cardiac fibrosis. In addition, the expression of prostaglandin E2 receptor 4 (EP4) was decreased in cardiac fibrosis. In vivo lnc000908 silencing by lentivirus increased the EP4 level, decreased endothelial-mesenchymal transition (EndMT) and improved cardiac fibrosis and cardiac function. Consistently, the lnc000908 knockdown also up-regulated EP4 and suppressed transforming growth factor-beta (TGF-β)-induced EndMT in cardiac microvascular endothelial cells. In contrast, the lnc000908 overexpression by lentivirus decreased the EP4 level and induced EndMT. Of note, these pro- or anti-EndMT effects were reversed by the EP4 overexpression or the EP4 antagonist AH-23848, respectively. This study demonstrates that lnc000908 is a novel regulator of cardiac fibrosis by modulating the EP4 expression and EndMT.
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