Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Wijermars 2016 Am J Transplant

From Bioblast
Publications in the MiPMap
Wijermars LG, Schaapherder AF, Kostidis S, Wรผst RC, Lindeman JH (2016) Succinate accumulation and ischemia reperfusion injury: of mice but not men - A study in renal ischemia reperfusion. Am J Transplant 16:2741-6.

ยป PMID: 26999803

Wijermars LG, Schaapherder AF, Kostidis S, Wuest Rob CI, Lindeman Jan HN (2016) Am J Transplant

Abstract: A recent seminal paper implicated ischemia-related succinate accumulation followed by succinate driven-reactive oxygen species formation as key driver of ischemia reperfusion injury. Although the data show that the mechanism is universal for all organs tested (kidney, liver, heart and brain), a remaining question is to what extend these observations for mouse translate to man. We here show that succinate accumulation is not a universal event during ischemia, and does not occur during renal graft procurement, in fact tissue succinate content progressively decreases with advancing graft ischemia time (p<0.007). Contrasting responses were also found with respect to mitochondrial susceptibility towards ischemia and reperfusion, with rodent mitochondria robustly resistant towards warm ischemia, but human and pig mitochondria being highly susceptible to warm ischemia (p<0.05). These observations suggest that succinate-driven reactive oxygen formation does not occur in the context of kidney transplantation. In fact absent allantoin release from the reperfused grafts suggests minimal oxidative stress during clinical reperfusion.

This article is protected by copyright. All rights reserved.


โ€ข O2k-Network Lab: NL Amsterdam Wuest RC, NL Leiden Lindeman JHN


Labels: MiParea: Respiration, Comparative MiP;environmental MiP, mt-Medicine 

Stress:Ischemia-reperfusion, Oxidative stress;RONS  Organism: Human, Pig, Mouse, Rat  Tissue;cell: Kidney  Preparation: Permeabilized tissue 


Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, NS, ROX  HRR: Oxygraph-2k 

2016-07