Scientists have managed to halt the progression of heart disease in mice, and even reverse some of its deleterious effects, by silencing, or blocking, a type of genetic material called microRNA.
In recent years, microRNA, a class of small non-coding RNAs that are involved in gene expression, has been implicated in the pathology of heart disease. Professor Eric Olson and colleagues have been studying the role of a particular microRNA, known as microRNA21 (miR-21), in cardiac fibroblasts, which help to provide the structure of the heart, and which play a crucial role in the progressive scarring of the heart that occurs in heart disease.
The scientists found that miR-21 regulates the ERK–MAP kinase signaling pathway in cardiac fibroblasts, which has a fundamental role on cardiac structure and function. They also found that miR-21 levels are increased in fibroblasts of failing hearts, and that this increases the activity of ERK–MAP kinase, thus causing more damage to the heart. However, silencing, or blocking, miR-21 in mice was found to reduce ERK-MAP kinase activity and improve cardiac function.
The authors concluded: “These findings reveal that microRNAs can contribute to myocardial disease by an effect in cardiac fibroblasts. Our results validate miR-21 as a disease target in heart failure and establish the therapeutic efficacy of microRNA therapeutic intervention in a cardiovascular disease setting.”
Thum T, Gross C, Fielder J, et al. MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts. Nature. Published online 30 November 2008. doi:10.1038/nature07511
