miR-155 in the Heart: The Right Time at the Right Place in the Right Cell
Cardiovascular complications arising as a consequence of vascular disease are on the rise in the world, with an urgent need to develop therapies that can prevent the drivers of atherosclerosis and promote healing of infarcted tissue following an ischemic event. Rupture of culprit atherosclerotic lesions is the main driver of downstream myocardial infarction (MI), accounting for 7 million deaths annually and 23 million individuals living with heart failure worldwide1. Accordingly, there has been a tremendous interest in using novel therapies to revascularize ischemic tissue and repair damaged myocardium following MI2. And while there is a clear clinical need to promote collateral vessel growth to facilitate healing and preserve tissue integrity following an ischemic event, the mechanisms that govern the growth of collateral vessels remain largely unknown. In this issue of Circulation, Pankratz3 and colleagues use microRNAs to study the different mechanisms that promote angiogenesis and arteriogenesis and find that miR-155 has dual and opposing roles in both processes.
- Received April 2, 2015.
- Accepted April 2, 2015.