Angioplasty is the most common medical intervention in the world today – more than 2 million coronary artery patients are treated each year with balloon dilations or stents to widen coronary arteries with the goal to restore normal blood flow to the heart. While the procedure is beneficial in the first place, restenosis is a frequent event in the months after the intervention. It occurs in 10-20% of patients who received coronary artery stents and in up to 50% of patients who had undergone balloon angioplasty. In patients receiving drug-eluting stents (DES), restenosis rate is about 5%. However, these stents in the long run pose the risk of thrombosis. So far, no causal treatment of restenosis is available.
Restenosis is caused by a physiological reaction that is trying to repair the damage induced by the angioplasty procedure. It develops by increased proliferation of vascular smooth muscles cells (VSMCs) in the vessel walls. VSMCs respond to changes in the local environment by adjusting their phenotype from contractile to synthetic, and failure of VSMCs to acquire and maintain the contractile phenotype plays a key role in this process.
Scientists from the Max Planck Institute for Heart and Lung Research have now developed a novel treatment approach. They found that small non-coding RNAs (miRNAs 143/145) specifically expressed in VSMCs control the cells’ phenotypic variation. Therefore, modulation of miRNAs 143/145 levels through activators or stents eluting miRNA 143/145 mimetics may be a very promising approach inhibit restenosis and/or to combat arteriosclerosis.
The technology is being offered by Max-Planck-Innovation.