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• W2517963807 abstract "EpigenomicsVol. 8, No. 10 EditorialmiRNA-140-5p: new avenue for pulmonary arterial hypertension drug development?Alexander MK Rothman, David J Rowlands & Allan LawrieAlexander MK Rothman Department of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, S10 2RX, UK Sheffield Teaching Hospitals NHS Trust, Sheffield, S10 2JF, UKSearch for more papers by this author, David J Rowlands Novartis Institutes for Biomedical Research, Cambridge, MA 02139, USASearch for more papers by this author & Allan Lawrie*Author for correspondence: E-mail Address: a.lawrie@sheffield.ac.uk Department of Infection, Immunity & Cardiovascular Disease, University of Sheffield, Sheffield, S10 2RX, UKSearch for more papers by this authorPublished Online:7 Sep 2016https://doi.org/10.2217/epi-2016-0089AboutSectionsView ArticleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinkedInReddit View articleKeywords: miR140-5pmiRNApulmonary arterial hypertensionremodelingSmurf1ubiquitinationReferences1 Schermuly RT, Ghofrani HA, Wilkins MR, Grimminger F. 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Systems-level regulation of microRNA networks by miR-130/301 promotes pulmonary hypertension. J. Clin. Invest. 124(8), 3514–3528 (2014).Crossref, Medline, CAS, Google Scholar15 Rhodes CJ, Wharton J, Boon RA et al. Reduced microRNA-150 is associated with poor survival in pulmonary arterial hypertension. Am. J. Respir. Crit. Care Med. 187(3), 294–302 (2013).Crossref, Medline, CAS, Google Scholar16 Schlosser K, Taha M, Deng Y, Jiang B, Stewart DJ. Discordant regulation of microRNA between multiple experimental models and human pulmonary hypertension. Chest 148(2), 481–410 (2015).Crossref, Medline, Google Scholar17 Rothman AMK, Arnold ND, Pickworth JA et al. MicroRNA-140-5p and SMURF1 regulate pulmonary arterial hypertension. J. Clin. Invest. 126(7), 2495–508 (2016).Crossref, Medline, Google Scholar18 Murakami K, Mathew R, Huang J et al. Smurf1 ubiquitin ligase causes downregulation of BMP receptors and is induced in monocrotaline and hypoxia models of pulmonary arterial hypertension. Exp. Biol. Med. (Maywood) 235(7), 805–813 (2010).Crossref, Medline, CAS, Google Scholar19 Zhu H, Kavsak P, Abdollah S, Wrana JL, Thomsen GH. A SMAD ubiquitin ligase targets the BMP pathway and affects embryonic pattern formation. Nature 400(6745), 687–693 (1999).Crossref, Medline, CAS, Google Scholar20 Landré V, Rotblat B, Melino S, Bernassola F, Melino G. Screening for E3-ubiquitin ligase inhibitors: challenges and opportunities. Oncotarget 5(18), 7988–8013 (2014).Crossref, Medline, Google Scholar21 Andrews PS, Schneider S, Yang E et al. Identification of substrates of SMURF1 ubiquitin ligase activity utilizing protein microarrays. Assay Drug Dev. Technol. 8(4), 471–487 (2010).Crossref, Medline, CAS, Google ScholarFiguresReferencesRelatedDetailsCited ByThe E3 ubiquitin ligases regulate inflammation in cardiovascular diseasesSeminars in Cell & Developmental Biology, Vol. 6An Overview of miRNAs Involved in PASMC Phenotypic Switching in Pulmonary HypertensionBioMed Research International, Vol. 2021MicroRNA‐140‐5p targeting tumor necrosis factor‐α prevents pulmonary arterial hypertension26 October 2018 | Journal of Cellular Physiology, Vol. 234, No. 6 Vol. 8, No. 10 Follow us on social media for the latest updates Metrics Downloaded 172 times History Published online 7 September 2016 Published in print October 2016 Information© Future Medicine LtdKeywordsmiR140-5pmiRNApulmonary arterial hypertensionremodelingSmurf1ubiquitinationAcknowledgementsThe authors would like to thank the patients and their families who provides samples to the Sheffield Pulmonary Hypertension Biobank.Financial & competing interests disclosureFunding for this research was provided by a Medical Research Council Clinical Research Training Fellowship (AMK Rothman: MR/K002406/1); Medical Research Council Career Development Award (A Lawrie: G0800318); British Heart Foundation Senior Basic Science Fellowship (A Lawrie: FS/13/48/30453) and British Heart Foundation Project Grant (PG/11/11629288). The collection of patient blood samples was coordinated through the Sheffield NIHR Clinical Research Facility. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.No writing assistance was utilized in the production of this manuscript.PDF download" @default.
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