Pro-inflammatory interleukin genotypes potentiate early and advanced atherosclerosis differently.


MicroRNAs (miRNAs) play an important role in the pathogenesis of structural alterations of cardiac hypertrophy (1). However, the precise mechanisms of miRNA-29a in cardiac hypertrophy are still unclear. A recent report in the Journal by Roncarati et al. (2) indicated that correlation with left ventricular hypertrophy parameters holds true for only miRNA29a, which is significantly associated with both cardiac hypertrophy and fibrosis. This suggests that miRNA-29a is a potential therapeutic target for cardiac hypertrophy. Other studies have found that down-regulation of miRNA-29a is associated with pathological cardiac hypertrophy. Abonnenc et al. (3) showed that levels of miRNA-29a were significantly reduced in a mouse model of pathological but not physiological hypertrophy (3). Furthermore, Divakaran et al. (4) indicated that Smad3 signaling plays dual roles in the heart: a beneficial role by delimiting hypertrophic growth and a deleterious role by modulating myocardial fibrosis, possibly through a pathway that entails accumulation of miRNA-29a, which decreases collagen gene expression. However, Zile et al. (5) showed that miRNA-29a levels increased 5 days after myocardial infarction and then decreased to control levels at later time points. A time-dependent change in miRNA-29a levels occurred in patients with myocardial infarction, including an early and robust increase in miRNA levels that affected myocardial fibrosis. These findings suggest that miRNA-29a may be a good clinical biomarker for patients with cardiac hypertrophy because it seems to play a key role in the development of this condition. Additional studies with more patients and animal studies are needed to determine the precise role of miRNA-29a in cardiac hypertrophy, and therapeutic agents targeting miRNA-29a might result in innovative new therapies. All in all, we greatly enjoyed reading the article by Roncarati et al. (2) and believe that miRNA-29a may be useful for the prevention and treatment of cardiac hypertrophy.

DOI: 10.1016/j.jacc.2014.05.043

Cite this paper

@article{Oikonomou2014ProinflammatoryIG, title={Pro-inflammatory interleukin genotypes potentiate early and advanced atherosclerosis differently.}, author={Evangelos Oikonomou and Gerasimos Siasos and Dimitris Tousoulis}, journal={Journal of the American College of Cardiology}, year={2014}, volume={64 8}, pages={848-9} }