Key result
Noncoding RNAs regulate cardiac fibrosis and myofibroblast activation, offering novel therapeutic targets.
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Cardiac fibrosis as a result of excessive extracellular matrix deposition leads to stiffening of the heart, which can eventually lead to heart failure. An important event in cardiac fibrosis is the transformation of fibroblasts into myofibroblasts, which secrete large amounts of extracellular matrix proteins. Although the function of protein-coding genes in myofibroblast activation and fibrosis have been a topic of investigation for a long time, it has become clear that noncoding RNAs also play key roles in cardiac fibrosis. This review discusses the involvement of microRNAs and long noncoding RNAs in cardiac fibrosis and summarizes the issues related to translating these findings into real-life therapies.
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Creemers et al. (2015) conducted a review in Cardiac fibrosis. Noncoding RNAs (microRNAs and long noncoding RNAs) was evaluated. Noncoding RNAs, specifically microRNAs and long noncoding RNAs, play key roles in cardiac fibrosis and myofibroblast activation, presenting potential avenues for future targeted therapies.
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