Abstract
Cardiac remodeling, which is characterized by mechanical and electrical remodeling, is a significant pathophysiological process involved in almost all forms of heart diseases. MicroRNAs (miRNAs) are a group of non-coding RNAs of 20–25 nucleotides in length that primarily regulate gene expression by promoting mRNA degradation or post-transcriptional repression in a sequence-specific manner. Three miR-133 genes have been identified in the human genome, miR-133a-1, miR-133a-2, and miR-133b, which are located on chromosomes 18, 20, and 6, respectively. These miRNAs are mainly expressed in muscle tissues and appear to repress the expression of non-muscle genes. Based on accumulating evidence, miR-133 participates in the proliferation, differentiation, survival, hypertrophic growth, and electrical conduction of cardiac cells, which are essential for cardiac fibrosis, cardiac hypertrophy, and arrhythmia. Nevertheless, the roles of miR-133 in cardiac remodeling are ambiguous, and the mechanisms are also sophisticated, involving many target genes and signaling pathways, such as RhoA, MAPK, TGFβ/Smad, and PI3K/Akt. Therefore, in this review, we summarize the critical roles of miR-133 and its potential mechanisms in cardiac remodeling.
Highlights
Heart failure (HF), a rapidly growing public health issue, had an estimated prevalence of over 37.7 million individuals worldwide in 2016, contributing to a grave disease burden (Ziaeian and Fonarow, 2016)
MicroRNAs are a class of small non-coding RNAs of approximately 20-25 nucleotides in length that are typically excised from putative miRNA precursor with 60–110 nucleotides and play vital biological roles by directly binding to the 3′ Untranslated regions (UTR) of target messenger RNAs (Pan et al, 2017)
We described the roles and mechanisms of miR133 in cardiac remodeling, which might be beneficial references for clinical applications and future investigations
Summary
Heart failure (HF), a rapidly growing public health issue, had an estimated prevalence of over 37.7 million individuals worldwide in 2016, contributing to a grave disease burden (Ziaeian and Fonarow, 2016). Cardiac remodeling is generally accepted as constant adjustments of the myocardium to the structure, metabolism and electrical conduction under the influence of various endogenous and exogenous factors, which eventually result in alterations in the ventricle structure and biological effects
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