CIRCULATIONAHA.119.042474.pdf (427.67 kB)
Regulatory RNAs in Heart Failure
journal contribution
posted on 2020-05-22, 12:36 authored by CPDC Gomes, B Schroen, GM Kuster, EL Robinson, K Ford, IB Squire, S Heymans, F Martelli, C Emanueli, Y DevauxCardiovascular disease is an enormous socioeconomic burden worldwide and remains a leading cause of mortality and disability despite significant efforts to improve treatments and personalize healthcare. Heart failure is the main manifestation of cardiovascular disease and has reached epidemic proportions. Heart failure follows a loss of cardiac homeostasis, which relies on a tight regulation of gene expression. This regulation is under the control of multiple types of RNA molecules, some encoding proteins (the so-called messenger RNAs) and others lacking protein-coding potential, named noncoding RNAs. In this review article, we aim to revisit the notion of regulatory RNA, which has been thus far mainly confined to noncoding RNA. Regulatory RNA, which we propose to abbreviate as regRNA, can include both protein-coding RNAs and noncoding RNAs, as long as they contribute, directly or indirectly, to the regulation of gene expression. We will address the regulation and functional role of messenger RNAs, microRNAs, long noncoding RNAs, and circular RNAs (ie, regRNAs) in heart failure. We will debate the utility of regRNAs to diagnose, prognosticate, and treat heart failure, and we will provide directions for future work.
Funding
This publication is based upon work from the EU-CardioRNA COST ACTION CA17129, supported by COST (European Cooperation in Science and Technology). The open access fee of this publication was supported by EU-CardioRNA COST ACTION CA17129. Y.D. is funded by the Ministry of Higher Education and Research, the Society for Research on Cardiovascular Disease, and the National Research Fund of Luxembourg (grant C17/BM/11613033). C.P.C.G. is funded by the Eurostars project MIPROG (grant EUROSTARS E! 9686). G.M.K. received funding from the Swiss National Science Foundation (310030_156953). S.H. received funding from the European Union Commission’s Seventh Framework programme under grant agreement N° 305507 (HOMAGE), N° 602904 (FIBROTARGETS) and N° 261409 (MEDIA) and N° 278249 (EU MASCARA); the Marie-Curie Industry Academy Pathways and Partnerships (CARDIOMIR) N°285991, FP7-Health-2013-Innovations-1 N° 602156 (HECATOS); the Netherlands Organization for Scientific Research (NWO) Vidi 91796338; the Netherlands Cardiovascular Research Initiative, an initiative with support of the Dutch Heart Foundation, CVON2016-Early HFPEF, 2015-10, and CVON She-PREDICTS, grant 2017–21, CVON-Arena-PRIME. B.S. is supported by grants from the Netherlands Heart Foundation (Dekker 2014T105 and CVON-SHE-PREDICTS-HF), Netherlands Organisation for Scientific Research (NWO vidi 917.14.363) and Health Foundation Limburg. F.M. is supported by Ministero della Salute (Ricerca Corrente, 5X1000). C.E. received funding from a British Heart Foundation programme grant “microRNAs from cardiac surgery to basic science–and back?” (RG/15/5/31446) and a British Heart Foundation Chair in Cardiovascular Science (CH/15/1/31199). E.L.R. received funding from CVON RECONNECT Talent programme grant, a Netherlands CardioVascular Research Initiative supported by the Hartstichting (Dutch Heart Foundation).
History
Citation
Circulation. 2020;141:313–328Version
- VoR (Version of Record)
