Atherosclerotic plaque is one of the leading causes of cardiovascular disease and researchers have been working on how to stop the root cause of its buildup which is inflammation. A new approach involving synthetic peptides could inhibit the effects of chemokines on arterial inflammation while sparing their role in essential physiological processes.
Anti-inflammatory therapies are complex
Developing new anti-inflammatory therapies for atherosclerosis is difficult. Still, researchers in Munich have just developed synthetic peptides that can inhibit the mechanisms that promote this disease. Their work was published in the journal Nature.
Atherosclerosis is a chronic inflammatory disease that affects artery walls through the action of mediators such as cytokines and chemokines that promote vascular inflammation. To prevent the effects of these inflammations, such as atherosclerosis, myocardial infarction, or rheumatoid arthritis, antibodies and anti-inflammatory drugs, are the main drugs used, although there are sometimes limitations.
Munich researchers have developed synthetic peptides (groups of amino acids involved in biological processes in the body) that are able to mimic specific chemokine receptors and inhibit the mechanisms that promote atherosclerosis without interfering with the action of these chemokines in controlling important physiological processes. Previously used drugs acted on atherosclerosis but also suppressed the beneficial effects of chemokines in defense against infections.
Potential clinical applications
“Synthetic peptides, mini-CXCR4 mimics, are able to selectively discriminate between two different chemokines that have the same receptor as a target thus specifically blocking the signaling pathways underlying atherosclerosis,” said Afrodite Kapurniotu, professor of peptide biochemistry at the University of Munich.
This study was conducted in the laboratory on animal models of atherosclerosis. “But clinical applications seem possible, not least because peptide-based therapies are significantly less expensive than antibodies,” says Prof. Bernhagen of the Institute for Stroke Research at the University of Munich Hospital. The results obtained are seen by the researchers as a “proof of principle” showing that therapies based on mini-chemokine-receptor mimics are feasible and that this concept could also be applied to other chemokines. In other words, this strategy could be used to treat other inflammatory diseases.