Open AccessChronic allograft nephropathy is prevented by inhibition of platelet-derived growth factor receptor: tyrosine kinase inhibitors as a potential therapy
Author(s) -
Johanna Savikko,
Eero Taskinen,
E von Willebrand
Publication year - 2003
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/01.tp.0000062836.93496.ce
Subject(s) - platelet derived growth factor receptor , medicine , chronic allograft nephropathy , transplantation , platelet derived growth factor , imatinib , syngenic , tyrosine kinase inhibitor , kidney , growth factor , immunology , kidney transplantation , cancer research , pharmacology , receptor , myeloid leukemia , cancer
Chronic allograft nephropathy (CAN) is the primary reason for late allograft loss in kidney transplantation, and currently there is no treatment available for it. Platelet-derived growth factor (PDGF) is suggested to be a major mitogen mediating mesenchymal cell proliferation in CAN. It has been shown that PDGF is already induced at acute renal allograft rejection, indicating a link between acute rejection and subsequent development of CAN. However, the definite effect of PDGF on the pathogenesis of CAN is still unknown. We investigated the role of PDGF in CAN by inhibiting PDGF by imatinib (STI571), a selective PDGF receptor tyrosine kinase inhibitor.