Author + information
- Yao Dai, MD,
- Dongsheng Dai, MD and
- Jawahar L. Mehta, MD, PhD∗ ()
- ↵∗Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences, 4301 West Markham Street, Mail Slot 532, Little Rock, Arkansas 72205-7199
Myocardial fibrosis is characterized by pathological modification of myocardium, in which cardiomyocytes undergo apoptosis and the heart tissue is replaced by fibroblasts; this phenomenon is usually referred to as cardiac remodeling. However, the pathogenesis of myocardial fibrosis is still unclear despite advances in our understanding of the ischemic process.
MicroRNAs (miRs), small endogenous noncoding RNAs, have a well-documented role in the regulation of the cardiovascular system. miRs such as miR-29 and miR-21 have been shown to have a role in the genesis of myocardial fibrosis.
Roncarati et al. (1) measured a set of miRs in the plasma of patients with hypertrophic cardiomyopathy to understand which miRs can be regarded as biomarkers of this disease. Only miR-29a levels were found to correlate with cardiac fibrosis, along with several miRs related to cardiac hypertrophy. This discovery is significant in that it may help define patients who may develop fibrosis. However, it is important to know where miR-29a comes from and what types of cells, cardiomyocytes or fibroblasts, secrete it. Previous studies have shown the opposite effect of miR-29 in different types of cells (2–5). On one hand, miR-29 can promote cardiomyocyte apoptosis via down-regulation of antiapoptosis genes, such as Bcl-2, CDC42, and Tcl-1 (2–4); on the other hand, miR-29 can protect against fibrosis through inhibition of collagens released from extracellular matrix (5). Because the majority of cell types change from cardiomyocyte to myofibroblast phenotype during progression of cardiac remodeling, it is reasonable to hypothesize that up-regulation of miR-29a in the plasma of these patients is mainly due to cardiomyocyte apoptosis and not secretion from fibroblasts. It is also possible that the up-regulation of miR-29a in plasma reflects the body’s attempt to express more fibrosis-protective mediators to prevent adverse cardiac remodeling.
Cardiac remodeling is a complicated process that involves a number of molecular and pathological alterations (5). A simple measurement of miRs at one time point may not be enough to define molecular changes. Identification of miR-29a (and other miRs) in different cell types and at different time points is necessary before recognizing it as a biomarker for cardiac remodeling.
Please note: Douglas Mann, MD, served as Guest Editor for this paper.
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