Author + information
- Gianluigi Condorelli, MD, PhD∗ ()
- ↵∗Cardiovascular Research, Humanitas Research Hospital, University of Milan, Via Manzoni 56, 20089 Rozzano, Milan, Italy
We thank Dr. Dai and colleagues for their interest in our paper (1). As their letter suggests, it is possible that microRNA (miR)-29 is secreted by more than one cell type. However, our intention was not to address this question, which has been partly done and should be tackled further in other settings and with appropriate technologies (tissue-specific knockout mice, transgenic mice, and so on); we simply found a significant correlation between a few circulating miRs, in particular miR-29a, and the degree of cardiac fibrosis in patients with hypertrophic cardiomyopathy.
We therefore agree with the concept expressed in the letter by Dr. Dai and colleagues that miR-29s are expressed in many cell types, where it probably plays a critical regulatory role. As stated in the letter, this miR family has been found to be an important player not only in fibroblasts and fibrosis but also in regulating the functions of macrophages and other inflammatory and immune cell types. It is worth noting that inflammation precedes or accompanies fibrosis. Fibrosis and inflammation are therefore 2 highly correlated phenomena. It is also possible, even though not yet proven, that miR-29s play a role in cardiomyocytes. As previously noted, more experimental studies need to address these important questions. The published data today show that a nonselective, ubiquitous knockout of miR-29s affects cardiac fibrosis in mice. To determine which cell type is responsible for this phenomenon, miR-29 cell-specific knockout approaches are needed.
Please note: Douglas Mann, MD, served as Guest Editor for this paper.
- American College of Cardiology Foundation