Open AccessApoptosis and inflammation in renal reperfusion injury
Author(s) -
M.A.R.C. Daemen,
Bart de Vries,
Wim A. Buurman
Publication year - 2002
Publication title -
transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.45
H-Index - 204
eISSN - 1534-6080
pISSN - 0041-1337
DOI - 10.1097/00007890-200206150-00001
Subject(s) - inflammation , apoptosis , pathogenesis , organ transplantation , reperfusion injury , caspase , transplantation , medicine , immunology , effector , kidney , ischemia , programmed cell death , pathology , biology , biochemistry
Ischemia followed by reperfusion (I/R) has cardinal implications in the pathogenesis of organ transplantation and rejection. Apoptosis and inflammation are central mechanisms leading to organ damage in the course of renal I/R. General aspects of apoptosis, morphology, induction, and biochemistry are discussed. Activated caspases, the classical effector enzymes of apoptosis, are able to induce not only apoptosis but also inflammation after I/R in experimental models. This redefines the involvement of apoptosis in I/R injury toward a central and functional role in the development of organ damage. Our purpose is to assess aspects of apoptosis and inflammation in terms of involvement in the pathogenesis of I/R-induced organ damage. Moreover, the implications of recent experimental advances for diagnosis and treatment of renal I/R injury in clinical practice will be discussed.