Mechanisms of post-intervention arterial remodelling

Abstract

It has been appreciated over the past two decades that arterial remodelling, in addition to intimal hyperplasia, contributes significantly to the degree of restenosis that develops following revascularization procedures. Remodelling appears to be an adventitia-based process that is contributed to by multiple factors including cytokines and growth factors that regulate extracellular matrix or phenotypic transformation of vascular cells including myofibroblasts. In this review, we summarize the currently available information from animal models as well as clinical investigations regarding arterial remodelling. The factors that contribute to this process are presented with an emphasis on potential therapeutic methods to enhance favourable remodelling and prevent restenosis.

Figure 1

Definition of arterial remodelling following injury. In the studies cited in Tables 1–5, remodelling is often assessed by comparing the EEL (area, perimeter, or diameter) of the injured vessel in the presence and absence of a treatment that modulates a molecular factor.

Figure 2

Schematic of the molecular factors that affect arterial remodelling (see text for details). For simplicity, the effect of these factors on intimal hyperplasia is not displayed, and the ECM proteins involved in remodelling are represented by collagen. TGF-β1, transforming growth factor β1; SMC, smooth muscle cell; ROS, reactive oxygen species; MMPs, matrix metaloproteinases; TTGs, tissue transglutaminases; EEL, external elastic lamina; IEL, internal elastic lamina.