Abstract
The role of small, non-coding microRNAs (miRNAs) has recently emerged as fundamental in the regulation of the physiology of the cardiovascular system. Several specific miRNAs were found to be expressed in embryonic, postnatal, and adult cardiac tissues. In the present review, we will provide an overview about their role in controlling the different pathways regulating cell identity and fate determination. In particular, we will focus on the involvement of miRNAs in pluripotency determination and reprogramming, and specifically on cardiac lineage commitment and cell direct transdifferentiation into cardiomyocytes. The identification of cardiac-specific miRNAs and their targets provide new promising insights into the mechanisms that regulate cardiac development, function and dysfunction. Furthermore, due to their contribution in reprogramming, they could offer new opportunities for developing safe and efficient cell-based therapies for cardiovascular disorders.
Highlights
The role of small, non-coding microRNAs has recently emerged as fundamental in the regulation of the physiology of the cardiovascular system
This study demonstrated that valproic acid (VPA) was able to reprogram mouse fibroblasts by degrading Hdac2 protein
The overexpression of miR-145 in human ESC (hESC) by using a lentiviral vector resulted in an increase of the mesoderm-specific markers α-smooth muscle actin (SMA), Mixl1, NODAL and the ectoderm-specific markers β-III tubulin (TUJ1) and orthodenticle homeobox 2 (OTX2) [91]
Summary
MicroRNAs (miRNAs ) are a class of 19–25 nucleotide (nt) non coding RNAs, evolutionarily conserved in animals [1] They modulate gene expression post-transcriptionally by inhibiting translation and/or inducing specific mRNA degradation. Improving knowledge about the role of miRNAs may help finding new mechanisms and markers or targets for cardiovascular diseases Considering their function in controlling gene expression in cell fate determination, cellular proliferation and differentiation [16], miRNAs might represent suitable tools to modulate ex vivo the commitment of endogenous stem cells to specific lineage, in order to develop safe and efficient cell therapies for cardiovascular disorders. The complexity of miRNA-dependent gene regulatory circuits can be explained considering different key properties such as: each miRNA can regulate the expression of several hundred genes; individual 3' UTRs can have binding sites for multiple miRNAs, allowing cooperation between miRNAs; and miRNAs themselves can be modulated by feedback mechanisms promoted by the protein products of mRNA targets [5]
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