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Updated: Aug 2, 2026

Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
Published on: August 9, 2013
Apoptosis and inflammation in renal reperfusion injury
Marc A R C Daemen1, Bart de Vries, Wim A Buurman
1Department of General Surgery, University of Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands.
Abstract:
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.
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