Inhibition of MicroRNAs in Mice Can Attenuate Cardiovascular Stress


Normal mouse heart pictured on the left compared to the one of the right, which has cardiac hypertrophy.

Cardiac stress that’s caused by a heart attack or high blood pressure will frequently lead to pathological heart growth and eventually lead to heart failure. Researchers have discovered that two micro-scale RNA molecules, microRNA miR-212 and miR-132 play a role in this detrimental development in mice. When these molecules were inhibited, the mice were protected against pathological heart growth and failure. Researchers hope to adapt these findings and develop therapeutic approaches that would work in humans.


The scientists published their findings in the journal Nature Communications. Other symptoms, like respiratory distress and fatigue can accompany heart failure. High blood pressure of valvular heart defects will lead to cardiac hypertrophy, which in turn, once it has developed in a patient, will lead to heart failure since the heart muscles enlarge to boost pumping performance. The microRNAs are more prevalent in cardiac muscle cells of mice suffering from cardiac hypertrophy.

In order to determine the role of these microRNAs, researchers bred genetically modified mice that had an abnormally large number of these molecules in their heart muscle cells. The mice developed cardiac hypertrophy and lived for only three to six months whereas healthy mice had a lifespan of several years. They also switched off the microRNAs in other mice, which in turn had smaller hearts than healthy mice, but this didn’t affect their lifespans.

Scientists then subjected these mice to stress by narrowing the aorta to determine if they would develop cardiac hypertrophy, but they didn’t. This is basically a molecular approach to treat pathological heart growth and failure in mice.

Reference: “The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy” by Ahmet Ucar, Shashi K. Gupta, Jan Fiedler, Erdem Erikci, Michal Kardasinski, Sandor Batkai, Seema Dangwal, Regalla Kumarswamy, Claudia Bang, Angelika Holzmann, Janet Remke, Massimiliano Caprio, Claudia Jentzsch, Stefan Engelhardt, Sabine Geisendorf, Carolina Glas, Thomas G. Hofmann, Michelle Nessling, Karsten Richter, Mario Schiffer, Lucie Carrier, L. Christian Napp, Johann Bauersachs, Kamal Chowdhury and Thomas Thum, 25 September 2012, Nature Communications.
DOI: 10.1038/ncomms2090

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