Figure 1. Interactions of extracellular matrix proteins and smooth muscle cell integrins regulate their differentiation state.

The work of Wang and colleagues⁷ adds COMP to the repertoire of extracellular matrix (ECM) proteins whose binding to their adhesion receptors, primarily integrins, contributes to the maintenance of the quiescent state of differentiated SMC. Following injury and in atherosclerosis, new ECM proteins are detected that in vitro promote SMC migration and proliferation associated with the de-differentiated SMC phenotype. It is less clear what triggers the transition from the differentiated to de-differentiated phenotype. Future studies of distinct regulatory mechanisms controlling COMP expression and turnover may help determine key components of this transition. DDR1, discoidin domain receptor 1