Preconditioning, postconditioning, and remote conditioning in solid organ transplantation: basic mechanisms and translational applications

Selzner, Nazia; Boehnert, Markus; Selzner, Markus

doi:10.1016/j.trre.2011.07.003

Cited by 71 publications

(56 citation statements)

References 82 publications

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“…DPCPX abrogated these effects of IPC. These implicate the control of GSK-3β activity by Aktmediated Ser 9 -GSK-3β phosphorylation preserving the efficiency of oxidative phosphorylation and ROS-mediated cell death in the ability of A1R activation to mimic IPC in the liver.…”

mentioning

confidence: 79%

“…In livers, PC can reduce the release of transaminases, increase the survival of rodents after liver transplantation, and even improve human hepatic functions after major liver surgery in patients subjected to 30 min of ischemia [5][6][7][8]. Furthermore, IPC decreases liver injury after both warm and cold I/R [2,4,9,10]. Several mechanisms have been proposed for protection by IPC, including activation of adenosine receptors [11][12][13][14], increased nitric oxide production [15], activation of protein kinase C [16], up-regulation of heat shock proteins, and increased antioxidant capacity [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Adenosine receptors: regulatory players in the preservation of mitochondrial function induced by ischemic preconditioning of rat liver

Duarte

Amorim

Varela

et al. 2016

Purinergic Signalling

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Although adenosine A 1 receptors (A1R) have been associated to ischemic preconditioning (IPC), direct evidence for their ability to preserve mitochondrial function upon hepatic preconditioning is still missing and could represent a novel strategy to boost the quality of liver transplants. We tested if the A1R antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) prevented IPC in the liver and if the A1R agonist 2-chloro-N 6 -cyclopentyladenosine (CCPA) might afford a pharmacological preconditioning. Livers underwent a 120 min of 70% warm ischemia and 16 h of reperfusion (I/R), and the IPC group underwent a 5-min ischemic episode followed by a 10-min period of reperfusion before I/R. DPCPX or CCPA was administered intraperitoneally 2 h before IPC or I/R. The control of mitochondrial function emerged as the central element affected by IPC and controlled by endogenous A1R activation. Thus, livers from IPC-or CCPA-treated rats displayed an improved oxidative phosphorylation with higher state 3 respiratory rate, higher respiratory control ratio, increased ATP content, and decreased lag phase. IPC and CCPA also prevented the I/Rinduced susceptibility to calcium-induced mitochondrial permeability transition, the rate of reactive oxygen species (ROS) generation, and the decreased mitochondrial content of phospho-Ser 9 GSK-3β. DPCPX abrogated these effects of IPC. These implicate the control of GSK-3β activity by Aktmediated Ser 9 -GSK-3β phosphorylation preserving the efficiency of oxidative phosphorylation and ROS-mediated cell death in the ability of A1R activation to mimic IPC in the liver. In conclusion, the parallel between IPC and A1R-mediated preconditioning also paves the way to consider a putative therapeutic use of the later in liver transplants.

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mentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Adenosine receptors: regulatory players in the preservation of mitochondrial function induced by ischemic preconditioning of rat liver

Duarte

Amorim

Varela

et al. 2016

Purinergic Signalling

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“…Despite experimental evidence demonstrating a decrease in renal allograft injury and improvement of allograft function, 75 only one small-sized study thus far has evaluated the role of rIPC in human renal transplantation. rIPC, consisting of three 5-minute cycles of leg ischemia and 5 minutes of reperfusion in donors or recipients, failed to improve early renal function in patients receiving living-donor renal transplantation.…”

mentioning

confidence: 99%

Remote Ischemic Preconditioning and Renoprotection

Gassanov¹,

Nia

Caglayan³

et al. 2014

Journal of the American Society of Nephrology

118

106

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There is currently no effective prophylactic regimen available to prevent contrastinduced AKI (CI-AKI), a frequent and life-threatening complication after cardiac catheterization. Therefore, novel treatment strategies are required to decrease CI-AKI incidence and to improve clinical outcomes in these patients. Remote ischemic preconditioning (rIPC), defined as transient brief episodes of ischemia at a remote site before a subsequent prolonged ischemia/reperfusion injury of the target organ, is an adaptational response that protects against ischemic and reperfusion insult. Indeed, several studies demonstrated the tissue-protective effects of rIPC in various target organs, including the kidneys. In this regard, rIPC may offer a novel noninvasive and virtually cost-free treatment strategy for decreasing CI-AKI incidence. This review evaluates the current experimental and clinical evidence for rIPC as a potential renoprotective strategy, and discusses the underlying mechanisms and key areas for future research.

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“…Yet, the transduction of the rIC stimulus from the remote organ or tissue to the target organ is complex and several questions remain unanswered. The underlying intracellular mediators and effectors in rIC in the target cells are to a great extent similar to the established protective pathways induced by local IC [25,35]. …”

Section: Overview Of Protective Molecular Mechanismsmentioning

confidence: 99%

Molecular Mechanisms of Renal Ischemic Conditioning Strategies

et al. 2015

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Ischemia-reperfusion injury is the leading cause of acute kidney injury in a variety of clinical settings such as renal transplantation and hypovolemic and/or septic shock. Strategies to reduce ischemia-reperfusion injury are obviously clinically relevant. Ischemic conditioning is an inherent part of the renal defense mechanism against ischemia and can be triggered by short periods of intermittent ischemia and reperfusion. Understanding the signaling transduction pathways of renal ischemic conditioning can promote further clinical translation and pharmacological advancements in this era. This review summarizes research on the molecular mechanisms underlying both local and remote ischemic pre-, per- and postconditioning of the kidney. The different types of conditioning strategies in the kidney recruit similar powerful pro-survival mechanisms. Likewise, renal ischemic conditioning mobilizes many of the same protective signaling pathways as in other organs, but differences are recognized.

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Preconditioning, postconditioning, and remote conditioning in solid organ transplantation: basic mechanisms and translational applications

Cited by 71 publications

References 82 publications

Adenosine receptors: regulatory players in the preservation of mitochondrial function induced by ischemic preconditioning of rat liver

Adenosine receptors: regulatory players in the preservation of mitochondrial function induced by ischemic preconditioning of rat liver

Remote Ischemic Preconditioning and Renoprotection

Molecular Mechanisms of Renal Ischemic Conditioning Strategies

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