Abstract
Transplantation-associated arteriosclerosis (TAA), a complication of allotransplantation, remains the major limitation to the long-term survival of many solid organ transplant recipients. Over the last decade, particularly, our understanding of the pathogenesis of TAA grew significantly. Morphological, immunohistochemical, and molecular studies performed on human tissues combined with an expanding clinical, radiological and epidemiological database have improved our knowledge of the cellular and biochemical events that culminate in TAA. Studies using innovative animal models have added to what has been gleaned from the human studies, and allowed for trials of unique therapeutic strategies. Nonetheless, for cardiac transplant recipients, TAA continues to be the largest single cause of death after the first year post-transplantation [1]. Arteriosclerosis is also a feature of chronic renal transplant rejection [2] and chronic pulmonary allograft rejection [3], though in lung allografts it appears to be unassociated with any physiological consequences [4]. Since much of the literature regarding TAA focuses upon its manifestations in the transplanted heart, the following discussion will concentrate primarily upon TAA developing in cardiac allografts, also known as cardiac allograft vasculopathy (CAV).
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Zander, D.S. (2001). Transplantation-associated arteriosclerosis and inflammation. In: Mehta, J.L. (eds) Inflammatory and Infectious Basis of Atherosclerosis. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8239-2_4
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