Cardiac Fibrosis Revisited by MicroRNA Therapeutics

C ardiac fibrosis is a result of a variety of injurious insults of different causes 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 collagen. 1 A major role in this process has been attributed to various growth factors, proteolytic enzymes, angiogenic factors, and fibrogenic cytokines.1 MicroRNAs (miRNAs/miRs) have recently come into focus as powerful regulators of gene expression, and they fundamentally influence the pathogenesis of different pathological events, including cardiac fibrosis.2 miRNAs are small noncoding RNAs (Ϸ22 nucleotides) that lead to silencing of genetic information through posttranscriptional degradation of mRNA and translational inhibition of protein expression.3,4 miRNAs are highly conserved in different species and are thought to regulate Ն50% 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 processed further.3 Numerous studies 2,5 have underlined their critical importance for disease initiation and progression by influencing distinct disease-specific signal transduction pathways.