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Silencing of circHIPK3 Inhibits Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction by Sponging miR-185-3p
Author(s) -
Xiaohan Xu,
Junhong Wang,
Xiaowei Wang
Publication year - 2020
Publication title -
drug design, development and therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.964
H-Index - 64
ISSN - 1177-8881
DOI - 10.2147/dddt.s245199
Subject(s) - pressure overload , medicine , atrial natriuretic peptide , muscle hypertrophy , angiotensin ii , ejection fraction , gene silencing , gene knockdown , renin–angiotensin system , brain natriuretic peptide , endocrinology , heart failure , biology , cardiology , blood pressure , cardiac hypertrophy , gene , biochemistry
Cardiac hypertrophy is induced by diverse patho-physiological stimuli and indicates an increase in cardiomyocyte size. Circular RNAs (circRNAs) and microRNAs (miRNAs), members of noncoding RNAs, are involved in several biological processes and cardiovascular diseases (CVD). Here, we investigated the potential role of circHIPK3, which is produced by the third exon of the HIPK3 gene in cardiac hypertrophy.

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