Why the study?
Emerging evidence has demonstrated roles of lncRNAs in cardiac hypertrophy, prompting a review of recent research and potential therapeutic targets on lncRNA sites.
This review highlights the emerging role of lncRNAs in the pathophysiology of cardiac hypertrophy and their potential as targets for future gene therapies.
LncRNA modulation may emerge as a hypertrophy target; leaves open clinical translation pending interventional studies.
Cardiac hypertrophy is a typical pathological phenotype of cardiomyopathy and a result from pathological remodelling of cardiomyocytes in humans. At present, emerging evidence demonstrated the roles of long non-coding RNAs (lncRNAs) in regulating the pathophysiological process of cardiac hypertrophy. Herein, we would like to review the recent researches on this issue and try to analysis the potential therapeutic targets on lncRNA sites. Studies have revealed both genetic mutations related hypertrophic cardiomyopathy and the compensative cardiac hypertrophy due to pressure overload, inflammation, endocrine issues and other external stimulations, share a common molecular mechanism of ventricular hypertrophy. The emerging evidence identified the abnormal expression of lncRNAs would leading to the impairment the function of sarcomere, intracellular calcium handling and mitochondrial metabolisms. Several researches proved the therapeutic role of lncRNAs in preventing or reversing cardiac hypertrophy. With the development of delivery system for small pieces of oligonucleotide, clinicians could design gene therapy approaches to terminate the process of cardiac hypertrophy to provide better prognosis.
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Liu et al. (2020) studied this question.
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