Key result
MicroRNA modulation shows therapeutic promise for promoting cardiac repair and regeneration after MI.
Why the study?
The dysregulation of microRNAs during cardiac ischemia and their role in angiogenesis, fibrosis, and hypertrophy present therapeutic opportunities for heart repair after myocardial infarction, but understanding their expression patterns and localization is necessary for targeted treatment development.
MicroRNA modulation may enable future MI repair strategies; leaves open clinical translation pending rigorous trials.
MicroRNAs (miRNAs) are small, non-messenger RNAs, 20-22 nucleotides in size, which regulate gene expression at the post-transcriptional level. Typically, miRNAs target the 3' untranslated region (3'UTR) of mRNA transcripts leading to mRNA degradation or translational repression. The known dysregulation of miRNAs during cardiac ischemia and the crucial role of miRNA-dependent regulation of angiogenesis, fibrosis and hypertrophy present interesting therapeutic opportunities for repairing and regenerating the heart after myocardial infarction (MI). An understanding of the expression pattern and localization of deleterious and beneficial miRNAs during cardiac ischemia is necessary for the development of therapeutics designed to specifically treat the affected tissue and cell populations. This review focuses on the role and localization of key miRNAs implicated in MI while highlighting how their manipulation may promote cardiac repair.
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Chiarella-Redfern et al. (2015) conducted a review in Myocardial infarction. MicroRNAs (miRNAs) was evaluated. Manipulation of key microRNAs implicated in myocardial infarction presents therapeutic opportunities for promoting cardiac repair and regeneration.
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