Lymphangiogenesis in Chronic Rejection and Coronary Allograft Vasculopathy
An Emerging Diagnostic and Therapeutic Target?
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Article, see p 488
Although lymphatic endothelial cells comprise only 3% of the cells in the adult heart,1 the role of the lymphatic system in modulating cardiac disease has recently become the focus of significant research leading to an enhanced interest in the potential therapeutic manipulation of cardiac lymphangiogenesis.2,3 The current study by Edwards and colleagues4 in this issue of Circulation adds additional support for modulation of the cardiac lymphatic response to injury to attenuate disease progression. Cardiac allograft vasculopathy (CAV) remains the leading cause of death in patients >5 years posttransplant. This group presents enticing new evidence to suggest that enhanced lymphatic flow from donor transplant myocardium to local host lymph nodes and subsequent augmentation of antigen presentation are at least partially responsible for CAV. The authors used a minor antigen (HY) sex-mismatched murine heterotopic cardiac transplantation model combined with single-photon emission computed tomography lymphoscintigraphy to document increased lymphatic flow in sex-mismatched controls that correlated with an increase in the donor cell presentation to the mediastinal lymph nodes, increased lymphatic vessel area, and an increase in immunoreactive cells in the graft (Figure). These observations lead the authors to speculate that inhibition of lymphangiogenesis may dampen chronic rejection by attenuating efferent flow of donor antigen presenting cells to host lymph nodes.