Succinate accumulation drives ischaemia-reperfusion injury during organ transplantation

Ischaemia Reperfusion Injury in Kidney Transplantation

The disruption of an organ’s blood supply is obligatory in clinical transplantation occurring at the time of organ procurement. During this ischaemic period complex pathophysiological changes occur within the organ that leave it primed in a pro-inflammatory state. Although the re-establishment of blood flow is essential to halt ongoing ischaemic damage, the organ incurs additional injury. This ...

Anticoagulant therapy in critical organ ischaemia/reperfusion injury.

Ischaemia/reperfusion (I/R) injury is central to a number of pathologies including myocardial infarction and stroke. Several cellular processes are involved in the progress of I/R injury, involving complex interactions between coagulation and inflammatory or apoptotic processes. Besides for their anti-coagulant function, anticoagulant proteins such as activated protein C (APC), active site inhi...

Vascular ischaemia and reperfusion injury.

Although restoration of blood flow to an ischaemic organ is essential to prevent irreversible tissue injury, reperfusion per se may result in a local and systemic inflammatory response that may augment tissue injury in excess of that produced by ischaemia alone. Cellular damage after reperfusion of previously viable ischaemic tissues is defined as ischaemia-reperfusion (I-R) injury. I-R injury ...

Ischaemia-Reperfusion-Induced Kidney Injury

Endoglin regulates renal ischaemia-reperfusion injury.

BACKGROUND Renal ischaemia-reperfusion (I-R) can cause acute tubular necrosis and chronic renal deterioration. Endoglin, an accessory receptor for Transforming Growth Factor-beta1 (TGF-beta1), is expressed on activated endothelium during macrophage maturation and implicated in the control of fibrosis, angiogenesis and inflammation. METHODS Endoglin expression was monitored over 14 days after ...