Long non-coding RNAs in cardiac hypertrophy
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Long non-coding RNAs in cardiac hypertrophy Jinghui Sun 1 & Chenglong Wang 1
# Springer Science+Business Media, LLC, part of Springer Nature 2019
Abstract Cardiac hypertrophy (CH) is generally considered adaptive responses that may occur after myocardial infarction, pressure overload, volume overload, inflammatory heart muscle disease, or idiopathic dilated cardiomyopathy, whereas long-term stimulation eventually leads to heart failure (HF). However, the current molecular mechanisms involved in CH are unclear. Recently, increasing evidences reveal that long non-coding RNAs (lncRNAs) play vital roles in CH. Different lncRNAs can promote or inhibit the pathological process of CH by different mechanisms, while the regulation of lncRNAs expression can improve CH. Thus, CH-related lncRNAs may become a novel field of research on CH. Keywords Cardiac hypertrophy . Long non-coding RNAs . Heart failure . Cardiac remodeling
Introduction Cardiac hypertrophy (CH) is adaptive responses that often occur after myocardial infarction and pressure overload. Although the initially adaptive response can maintain cardiac output, persistent CH is often accompanied by maladaptive cardiac remodeling, resulting in decreased compliance, increased risk of heart failure (HF), and sudden death [1, 2]. The level of treatment is improving rapidly, but mortality rates of HF remain about 50% within 5 years of diagnosis [3]. Prevention of maladaptive CH is a crucial method for the treatment of HF. Many hormones and cytokines are proved to be involved in the regulation of CH [4], but the complete pathological molecular mechanism remains far from full unclear, which hinders the development of better treatments of CH. Moreover, negative modulators of the hypertrophic response are essential to maintain a balance between compensatory hypertrophy and uncontrolled progression. Therefore, identifying the key molecular mechanisms involved in CH is a vital challenge for treatment of HF. In the mammalian genome, protein-coding genes account for about 1.5%, while the non-coding RNAs (ncRNAs) take up most of the genome [5]. Long non-coding RNAs (lncRNAs) are major components of ncRNAs, whose * Chenglong Wang [email protected] 1
Cardiovascular Disease Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Haidian District, Beijing 100091, China
transcription products are longer than 200 nucleotides. Initially, lncRNAs were considered as genomic transcriptional noise, but later have been demonstrated to play vital roles in multiple biological behaviors [6] and are associated with the pathological process of many diseases [7]. The molecular mechanisms of lncRNAs are abundant, including structural scaffolds [8], RNA processing [9], marker of cell fate [10], chromatin modification [11], and as a competing endogenous RNA (ceRNA) [12]. Increasing evidences show that lncRNAs exert their function by regulating translation, splicing, and gene expression [6, 13]. Recently, the roles of lncRNAs in CH have been demonstrated through plentiful studies
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