Research ArticleAtherosclerosis

Neutrophil-Derived Cathelicidin Protects from Neointimal Hyperplasia

See allHide authors and affiliations

Science Translational Medicine  05 Oct 2011:
Vol. 3, Issue 103, pp. 103ra98
DOI: 10.1126/scitranslmed.3002531

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

A Narrow Escape for Stents

A heart-healthy diet may reduce your risk of atherosclerosis and heart attack, but what if the damage is already done? For severe cases of atherosclerosis, a cardiologist can implant a device called a stent to widen or even open a blocked artery. Ironically, however, stent implantation can activate an immune response, which leads to restenosis—a narrowing of the blood vessels that restricts flow. Stents that elute drugs such as antiproliferative or anti-inflammatory agents have decreased this risk, but at the same time, they increase the risk of blood clot formation. Now, Soehnlein et al. find that stents coated with an antimicrobial peptide produced by innate immune cells promote vascular healing.

In an animal model of atherosclerosis, the authors observed that neutrophils could decrease vessel narrowing by secreting the antimicrobial peptide cathelicidin (mouse CRAMP, human LL-37). When deposited by neutrophils at the site of vascular injury, CRAMP recruited new blood vessel–producing cells and promoted the regrowth of vascular endothelial cells in damaged regions. The authors then translated this observation to clinically applicable technology by coating vascular stents with cathelicidin. Indeed, cathelicidin-coated stents reduced in-stent restenosis in their mouse model of atherosclerosis. Although it remains to be seen whether this effect will be reproduced in humans, cathelicidin coating may prevent stents from causing the very problem they’re supposed to treat and thus improve therapy for severe atherosclerosis.

Footnotes

  • * These authors contributed equally to this work.

View Full Text