Growth factors, cytokines, and vascular injury

Restenosis after angioplasty can be considered as the undesirable consequence of the vascular response to injury. The repair process, which manifests as smooth muscle cell hyperplasia and extracellular matrix deposition, is controlled by growth factors and cytokines from a variety of sources. Vascular smooth muscle cells themselves synthesize mitogens, such as platelet-derived growth factor and insulinlike growth factor I, which synergize to promote medial cell proliferation. Additionally, growth factors such as fibroblast growth factor are probably released by trauma from damaged smooth muscle cells or from the matrix that surrounds them. The abundance and cellular distribution of cell membrane receptors for the various growth factors is also modulated after arterial injury, and probably plays a role in determining the characteristics and magnitude of the proliferative response. It is becoming increasingly apparent that multiple redundant and often overlapping control mechanisms are involved in modulating restenosis. As the sequence of signaling events is unraveled, and antagonists to the critical mediators are developed, it is likely that more effective treatment protocols will become available to improve the long-term outcome of angioplasty procedures.