Cardiac allograft vasculopathy (CAV) is a major source of late posttransplant mortality.
Although numerous cell types are implicated in the pathogenesis of CAV, it is unclear which
cells actually induce the vascular damage that results in intimal proliferation. Because
macrophages are abundant in CAV lesions and are capable of producing growth factors
implicated in neointimal proliferation, they are leading end-effector candidates.
Macrophages were depleted in a murine heterotopic cardiac transplant system known to …