Therapeutic targets in the treatment of allograft fibrosis.

摘要: The dramatic improvements in short-term graft survival and acute rejection rates could only have been dreamed of 20 years ago. Late loss following kidney transplantation is now the critical issue this decade. Frequently, associated with development tubular atrophy interstitial fibrosis within (i.e. chronic allograft nephropathy; CAN). Major treatment strategies disorder are non-specific focus intervention has on limiting injurious events. Following injury a fibrogenesis phase featuring both proliferative infiltrative responses mediated by chemokines, cytokines growth factors. In particular, TGFbeta strongly implicated pathogenesis epithelial-mesenchymal transformation (EMT) may be part process. cascade events results matrix accumulation, due to either increased production and/or reduced degradation matrix. Recent investigations into tissue suggested number new ameliorate synthesis. While majority therapies focused TGFbeta, not an ideal maneuver transplant settings alternative targets identified other fibrotic diseases will discussed. Attacking should organ transplantation.