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      Long non-coding RNAs in the failing heart and vasculature

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          Abstract

          Following completion of the human genome, it became evident that the majority of our DNA is transcribed into non-coding RNAs (ncRNAs) instead of protein-coding messenger RNA. Deciphering the function of these ncRNAs, including both small- and long ncRNAs (lncRNAs), is an emerging field of research. LncRNAs have been associated with many disorders and a number have been identified as key regulators in the development and progression of disease, including cardiovascular disease (CVD). CVD causes millions of deaths worldwide, annually. Risk factors include coronary artery disease, high blood pressure and ageing. In this review, we will focus on the roles of lncRNAs in the cellular and molecular processes that underlie the development of CVD: cardiomyocyte hypertrophy, fibrosis, inflammation, vascular disease and ageing. Finally, we discuss the biomarker and therapeutic potential of lncRNAs.

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          Most cited references143

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          Long noncoding RNA as modular scaffold of histone modification complexes.

          Long intergenic noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. Here, we show that the lincRNA HOTAIR serves as a scaffold for at least two distinct histone modification complexes. A 5' domain of HOTAIR binds polycomb repressive complex 2 (PRC2), whereas a 3' domain of HOTAIR binds the LSD1/CoREST/REST complex. The ability to tether two distinct complexes enables RNA-mediated assembly of PRC2 and LSD1 and coordinates targeting of PRC2 and LSD1 to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. Our results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, thereby specifying the pattern of histone modifications on target genes.
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            RNA maps reveal new RNA classes and a possible function for pervasive transcription.

            Significant fractions of eukaryotic genomes give rise to RNA, much of which is unannotated and has reduced protein-coding potential. The genomic origins and the associations of human nuclear and cytosolic polyadenylated RNAs longer than 200 nucleotides (nt) and whole-cell RNAs less than 200 nt were investigated in this genome-wide study. Subcellular addresses for nucleotides present in detected RNAs were assigned, and their potential processing into short RNAs was investigated. Taken together, these observations suggest a novel role for some unannotated RNAs as primary transcripts for the production of short RNAs. Three potentially functional classes of RNAs have been identified, two of which are syntenically conserved and correlate with the expression state of protein-coding genes. These data support a highly interleaved organization of the human transcriptome.
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              Cellular senescence in aging and age-related disease: from mechanisms to therapy.

              Cellular senescence, a process that imposes permanent proliferative arrest on cells in response to various stressors, has emerged as a potentially important contributor to aging and age-related disease, and it is an attractive target for therapeutic exploitation. A wealth of information about senescence in cultured cells has been acquired over the past half century; however, senescence in living organisms is poorly understood, largely because of technical limitations relating to the identification and characterization of senescent cells in tissues and organs. Furthermore, newly recognized beneficial signaling functions of senescence suggest that indiscriminately targeting senescent cells or modulating their secretome for anti-aging therapy may have negative consequences. Here we discuss current progress and challenges in understanding the stressors that induce senescence in vivo, the cell types that are prone to senesce, and the autocrine and paracrine properties of senescent cells in the contexts of aging and age-related diseases as well as disease therapy.
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                Author and article information

                Contributors
                Journal
                Noncoding RNA Res
                Noncoding RNA Res
                Non-coding RNA Research
                KeAi Publishing
                2468-0540
                14 April 2018
                September 2018
                14 April 2018
                : 3
                : 3
                : 118-130
                Affiliations
                [a ]Department of Cardiology, CARIM School for Cardiovascular Diseases, Maastricht University, Universiteitssingel 50, 6200 MD, Maastricht, The Netherlands
                [b ]Department of Physiology, CARIM School for Cardiovascular Diseases, Maastricht University, Universiteitssingel 50, 6200 MD, Maastricht, The Netherlands
                Author notes
                []Corresponding author. b.schroen@ 123456maastrichtuniversity.nl
                Article
                S2468-0540(17)30046-X
                10.1016/j.ncrna.2018.04.002
                6114261
                04de4c8f-40b4-42b5-a86e-ad0e089df7d1
                © 2018 Production and hosting by Elsevier B.V. on behalf of KeAi Communications Co., Ltd.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 31 October 2017
                : 9 April 2018
                : 9 April 2018
                Categories
                Article

                lncrna,cardiac disease,hypertrophy,fibrosis,inflammation,endothelial dysfunction,ageing

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