Although advances in graft procurement, preservation, matching and immunosuppression have all contributed to todays outstanding short-term graft survival rates after solid organ transplantation, similar success has not been achieved in preventing chronic transplant dysfunction (CTD) and extending long-term graft survival. CTD is being recognized as one of the major causes of long-term ( > 5 years) graft loss. CTD is featured by obliteration of the vascular lumen as a result of occlusive neointima formation referred to as transplant arteriopathy (TA). Uncontrolled proliferation (hyperplasia) of smooth muscle cells (SMCs) is in major part responsible for neointima formation in TA. Endothelial cells (ECs) cover the neointima and form the barrier between the circulating blood and the vascular wall. The etiology of TA is largely unknown and development of TA is refractory to most anti-rejection therapies. Recent data attribute an important role to host-derived vascular progenitor cells in the development of TA, and these cells may be recruited from various sources including the bone marrow. Vascular progenitor cells are potential targets for therapeutic intervention to attenuate TA development. Therefore, understanding the molecular pathways that promote recruitment of vascular progenitor cells, that determine their differentiation fate, and that determine the proliferative capacity of their progeny, is warranted to dissect their detrimental and possible beneficial effects in the development of TA.
Keywords: Arteriopathy, endothelium, progenitor cell, rejection, smooth muscle, stem cell, transplantation
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