Cardiac Fibrosis Revisited by MicroRNA Therapeutics
Cardiac fibrosis is a result of a variety of injurious insults of different etiologies to cardiac tissue, which ultimately culminates in destruction of physiological tissue architecture and progressive organ dysfunction. Histologically, it is characterized by activation/proliferation of fibroblasts and excessive matrix deposition including collagen1. A major role in this process has been attributed to various growth factors, proteolytic enzymes, angiogenic factors, and fibrogenic cytokines1. MicroRNAs (miRNAs/miRs) have recently come into focus as powerful regulators of gene expression and fundamentally impact on the pathogenesis of different pathological events, including cardiac fibrosis2. MiRNAs are small non-coding RNAs (~22 nucleotides) that lead to silencing of genetic information through post-transcriptional degradation of messenger-RNA and/or translational inhibition of protein expression3,4. MiRNAs are highly conserved in different species and are thought to regulate at least 50% of the genome. MiRNAs are formed in a highly regulated process in the nucleus and are then transported into the cytosol, in which they are further processed3. Numerous studies have underlined their critical importance for disease initiation and progression by influencing distinct disease-specific signal transduction pathways2,5. (SELECT FULL TEXT TO CONTINUE)
- Received July 10, 2012.
- Accepted July 11, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited