Elastin degradation and ensuing inflammation as emerging keys to atherosclerosis

Abstract

This editorial refers to ‘Elastin-derived peptides potentiate atherosclerosis through the immune Neu1–PI3Kγ pathway’ by S. Gayral et al. , pp. 118–127, this issue. In atherosclerosis, remodelling of extracellular matrix (ECM) has long been considered a critical step in disease development/progression, but the multitude of cell types and molecular mechanisms involved is only now starting to emerge. In arteriosclerotic vascular disease, infiltrating leucocytes are known to release proteases, degrade the ECM, and lead to environmental changes allowing smooth muscle growth and plaque evolution. Among the enzymes secreted by leucocytes, a major role is played by elastases, which promote degradation of the elastin ring of arterial walls. This process triggers a tissue rearrangement that is more extensive than simple ECM destruction, because it triggers the production of elastin-derived peptides (EPs) that are not only degradation products, but also bioactive moieties evoking reactions in the surrounding tissues.1 EPs, also known as elastokines, are a family of matrix fragments that possess cytokine-like functions and primarily signal via binding to a unusual cell surface receptor, the elastin receptor …