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Abstract
Cardiac hypertrophy, characterized by the enlargement of cardiomyocytes, is initially an adaptive response to physiological and pathological stimuli. Decompensated cardiac hypertrophy is related to fibrosis, inflammatory cytokine, maladaptive remodeling, and heart failure. Although pathological myocardial hypertrophy is the main cause of hypertrophy-related morbidity and mortality, our understanding of its mechanism is still poor. Long noncoding RNAs (lncRNAs) are noncoding RNAs that regulate various physiological and pathological processes through multiple molecular mechanisms. Recently, accumulating evidence has indicated that lncRNA-H19 is a potent regulator of the progression of cardiac hypertrophy. For the first time, this review summarizes the current studies about the role of lncRNA-H19 in cardiac hypertrophy, including its pathophysiological processes and underlying pathological mechanism, including calcium regulation, fibrosis, apoptosis, angiogenesis, inflammation, and methylation. The context within which lncRNA-H19 might be developed as a target for cardiac hypertrophy treatment is then discussed to gain better insight into the possible biological functions of lncRNA-H19 in cardiac hypertrophy.
Highlights
Hypertrophic cardiomyopathy (HCM) is a common inherited disease characterized by an increase in the thickness of the ventricular wall (≥ 1.5 cm) in the absence of increased afterload, and it is recognized as an important cause of sudden cardiac death among young adults and competitive athletes [1]
The expression of H19 and miR-675 were found to be upregulated in pathological cardiac hypertrophy, and calmodulin-dependent protein kinase IIδ (CaMKIIδ) was shown to be a direct target of miR-675 and to partially mediate the effect of H19 on cardiomyocytes, indicating that miR-675-regulated CaMKIIδ might mediate the H19-induced inhibition of cardiomyocyte hypertrophy
Compared with most Long noncoding RNAs (lncRNAs), H19 is a locus with a high degree of sequence conservation in mammals, which means that H19 has important functions and may be a potential therapeutic possibility as a targeting molecule in HCM
Summary
Hypertrophic cardiomyopathy (HCM) is a common inherited disease characterized by an increase in the thickness of the ventricular wall (≥ 1.5 cm) in the absence of increased afterload, and it is recognized as an important cause of sudden cardiac death among young adults and competitive athletes [1]. Many studies have shown that lncRNAs are important regulators in many pathophysiological processes of heart development and diseases [22, 46, 47], such as cardiac organogenesis [48], atherosclerosis [49–51], hypertension [38, 52, 53], pulmonary arterial hypertension [54], coronary artery disease [55, 56], ischemia/reperfusion-induced apoptosis [57], HF [58], and CH (Table 1).
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