Fig. 5

Changes in extracellular matrix (ECM) during vascular remodelling. The increase in collagen crosslinking is mediated by lysyl oxidase (LOX) and LOX-like enzymes, whereas activated proteases, such as matrix metalloproteinases and serine elastase, induce ECM degradation and activation of growth factors, such as transforming growth factor-beta and fibroblast growth factor. Consequently, this activation stimulates vascular smooth muscle cells and fibroblasts to enhance the deposition of collagen, fibronectin, and tenascin, among others. After injury, the endothelial cell barrier function is impaired, leading to increased permeability, which allows unidentified serum factors to enter the vessel wall, stimulating arterial SMCs to secrete serine elastase and cause ECM degradation, forming a positive feedback loop